Publications by authors named "Mingsong Wang"

55 Publications

Genetic screens identify a context-specific PI3K/p27Kip1 node driving extrahepatic biliary cancer.

Cancer Discov 2021 Jul 19. Epub 2021 Jul 19.

Institute of Cancer Sciences, University of Glasgow.

Biliary tract cancer ranks among the most lethal human malignancies, representing an unmet clinical need. Its abysmal prognosis is tied to an increasing incidence and a fundamental lack of mechanistic knowledge regarding the molecular basis of the disease. Here, we show that the Pdx1-positive extrahepatic biliary epithelium is highly susceptible towards transformation by activated Pik3caH1047R, but refractory to oncogenic KrasG12D. Using genome-wide transposon screens and genetic loss-of-function experiments, we discover context-dependent genetic interactions that drive extrahepatic cholangiocarcinoma (ECC) and show that PI3K-signaling output strength and repression of the tumor-suppressor p27Kip1 are critical context-specific determinants of tumor formation. This contrasts the pancreas, where oncogenic Kras in concert with Trp53-loss are key cancer-drivers. Notably, inactivation of p27Kip1 permits KrasG12D-driven ECC development. These studies provide a mechanistic link between PI3K-signaling, tissue-specific tumor suppressor barriers, and ECC pathogenesis, and present a novel genetic model of autochthonous ECC and genes driving this highly lethal tumor-subtype.
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http://dx.doi.org/10.1158/2159-8290.CD-21-0209DOI Listing
July 2021

Comprehensive analysis of tumor microenvironment and identification of an immune signature to predict the prognosis and immunotherapeutic response in lung squamous cell carcinoma.

Ann Transl Med 2021 Apr;9(7):569

Department of Thoracic Surgery, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.

Background: Tumor mutation burden (TMB) and immune microenvironment are important determinants of prognosis and immunotherapeutic efficacy for cancer patients. The aim of the present study was to develop an immune signature to effectively predict prognosis and immunotherapeutic response in patients with lung squamous cell carcinoma (LUSC).

Methods: TMB and immune microenvironment characteristics were comprehensively analyzed by multi-omics data in LUSC. The immune signature was further constructed and validated in multiple independent datasets by LASSO Cox regression analysis. Next, the value of immune signature in predicting the response of immunotherapy was evaluated. Finally, the possible mechanism of immune signature was also investigated.

Results: A novel immune signature based on 5 genes was constructed and validated to predict the prognosis of LUSC patients. These genes were filamin-C, Rho family GTPase 1, interleukin 4-induced gene-1, transglutaminase 2, and prostaglandin I2 synthase. High-risk patients had significantly poorer survival than low-risk patients. A nomogram was also developed based on the immune signature and tumor stage, which showed good application. Furthermore, we found that the immune signature had a significant correlation with immune checkpoint, microsatellite instability, tumor infiltrating lymphocytes, cytotoxic activity scores, and T-cell-inflamed score, suggesting low-risk patients are more likely to benefit from immunotherapy. Finally, functional enrichment and pathway analyses revealed several significantly enriched immune-related biological processes and metabolic pathways.

Conclusions: In the present study, we developed a novel immune signature that could predict prognosis and immunotherapeutic response in LUSC patients. The results not only help identify LUSC patients with poor survival, but also increase our understanding of the immune microenvironment and immunotherapy in LUSC.
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http://dx.doi.org/10.21037/atm-21-463DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8105790PMC
April 2021

Directional Modulation of Exciton Emission Using Single Dielectric Nanospheres.

Adv Mater 2021 May 9;33(20):e2007236. Epub 2021 Apr 9.

Walker Department of Mechanical Engineering and Texas Materials Institute, The University of Texas at Austin, Austin, TX, 78712, USA.

Coupling emitters with nanoresonators is an effective strategy to control light emission at the subwavelength scale with high efficiency. Low-loss dielectric nanoantennas hold particular promise for this purpose, owing to their strong Mie resonances. Herein, a highly miniaturized platform is explored for the control of emission based on individual subwavelength Si nanospheres (SiNSs) to modulate the directional excitation and exciton emission of 2D transition metal dichalcogenides (2D TMDs). A modified Mie theory for dipole-sphere hybrid systems is derived to instruct the optimal design for desirable modulation performance. Controllable forward-to-backward intensity ratios are experimentally validated in 532 nm laser excitation and 635 nm exciton emission from a monolayer WS . Versatile light emission control is achieved for different emitters and excitation wavelengths, benefiting from the facile size control and isotropic shape of SiNSs. Simultaneous modulation of excitation and emission via a single SiNS at visible wavelengths significantly improves the efficiency and directionality of TMD exciton emission and leads to the potential of multifunctional integrated photonics. Overall, the work opens promising opportunities for nanophotonics and polaritonic systems, enabling efficient manipulation, enhancement, and reconfigurability of light-matter interactions.
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http://dx.doi.org/10.1002/adma.202007236DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8211409PMC
May 2021

Near-Field Characterization of Higher-Order Topological Photonic States at Optical Frequencies.

Adv Mater 2021 May 18;33(18):e2004376. Epub 2021 Mar 18.

Department of Electrical Engineering, Grove School of Engineering, City College of the City University of New York, 140th Street and Convent Avenue, New York, NY, 10031, USA.

Higher-order topological insulators (HOTIs) represent a new type of topological system, supporting boundary states localized over boundaries, two or more dimensions lower than the dimensionality of the system itself. Interestingly, photonic HOTIs can possess a richer physics than their original condensed matter counterpart, supporting conventional HOTI states based on tight-binding coupling, and a new type of topological HOTI states enabled by long-range interactions. Here, a new mechanism to establish all-dielectric infrared HOTI metasurfaces exhibiting both types of HOTI states is proposed, supported by a topological transition accompanied by the emergence of topological Wannier-type polarization. Two kinds of near-field experimental studies are performed: i) the solid immersion spectroscopy and ii) near-field imaging using scattering scanning near-field optical microscopy to directly observe the topological transition and the emergence of HOTI states of two types. It is shown that the near-field profiles indicate the displacement of the Wannier center across the topological transition leading to the topological dipole polarization and emergence of the topological boundary states. The proposed all-dielectric HOTI metasurface offers a new approach to confine the optical field in micro- and nano-scale topological cavities and thus paves the way to achieve a novel nanophotonic technology.
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http://dx.doi.org/10.1002/adma.202004376DOI Listing
May 2021

The long intergenic noncoding RNA GAS5 reduces cisplatin-resistance in non-small cell lung cancer through the miR-217/LHPP axis.

Aging (Albany NY) 2021 01 8;13(2):2864-2884. Epub 2021 Jan 8.

Department of Thoracic Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China.

Long noncoding RNAs (lncRNAs) are known to exert their effects to tumor progression. In this study, the role of the lncRNA GAS5 (growth arrest specific 5) was confirmed in reducing non-small cell lung cancer (NSCLC) cisplatin (DDP) resistance. In NSCLC tissue samples, GAS5 expression decreased significantly. Low GAS5 levels were positively correlated with NSCLC characteristics including TNM, tumor size and lymphatic metastasis. Functionally, GAS5 significantly reduced NSCLC/DDP cell migration, invasion and epithelial-mesenchymal transition (EMT) progression . , GAS5 upregulation inhibited remarkably NSCLC/DDP cell tumor growth. Mechanism analysis suggested that GAS5 was a molecular sponge of miR-217, inhibiting the expression of phospholysine phosphohistidine inorganic pyrophosphate phosphatase (LHPP). In conclusion, this study reveals that the GAS5/miR-217/LHPP pathway reduces NSCLC cisplatin resistance and that LHPP may serve as a potential therapeutic target for NSCLC cisplatin resistance.
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http://dx.doi.org/10.18632/aging.202352DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7880381PMC
January 2021

Tunable Chiral Optics in All-Solid-Phase Reconfigurable Dielectric Nanostructures.

Nano Lett 2021 01 29;21(2):973-979. Epub 2020 Dec 29.

Materials Science and Engineering Program, Texas Materials Institute, and Walker Department of Mechanical Engineering, The University of Texas at Austin, Austin, Texas 78712, United States.

Subwavelength nanostructures with tunable compositions and geometries show favorable optical functionalities for the implementation of nanophotonic systems. Precise and versatile control of structural configurations on solid substrates is essential for their applications in on-chip devices. Here, we report all-solid-phase reconfigurable chiral nanostructures with silicon nanoparticles and nanowires as the building blocks in which the configuration and chiroptical response can be tailored on-demand by dynamic manipulation of the silicon nanoparticle. We reveal that the optical chirality originates from the handedness-dependent coupling between optical resonances of the silicon nanoparticle and the silicon nanowire via numerical simulations and coupled-mode theory analysis. Furthermore, the coexisting electric and magnetic resonances support strong enhancement of optical near-field chirality, which enables label-free enantiodiscrimination of biomolecules in single nanostructures. Our results not only provide insight into the design of functional high-index materials but also bring new strategies to develop adaptive devices for photonic and electronic applications.
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http://dx.doi.org/10.1021/acs.nanolett.0c03957DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7855985PMC
January 2021

Suppressing material loss in the visible and near-infrared range for functional nanophotonics using bandgap engineering.

Nat Commun 2020 Oct 7;11(1):5055. Epub 2020 Oct 7.

Walker Department of Mechanical Engineering and Texas Materials Institute, The University of Texas at Austin, Austin, TX, 78712, USA.

All-dielectric nanostructures have recently opened exciting opportunities for functional nanophotonics, owing to their strong optical resonances along with low material loss in the near-infrared range. Pushing these concepts to the visible range is hindered by their larger absorption coefficient, thus encouraging the search for alternative dielectrics for nanophotonics. Here, we employ bandgap engineering to synthesize hydrogenated amorphous Si nanoparticles (a-Si:H NPs) offering ideal features for functional nanophotonics. We observe significant material loss suppression in a-Si:H NPs in the visible range caused by hydrogenation-induced bandgap renormalization, producing strong higher-order resonant modes in single NPs with Q factors up to ~100 in the visible and near-IR range. We also realize highly tunable all-dielectric meta-atoms by coupling a-Si:H NPs to photochromic spiropyran molecules. ~70% reversible all-optical tuning of light scattering at the higher-order resonant mode under a low incident light intensity is demonstrated. Our results promote the development of high-efficiency visible nanophotonic devices.
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http://dx.doi.org/10.1038/s41467-020-18793-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7542432PMC
October 2020

Reverse "L" surgical approach for the management of giant tumors of the cervicothoracic junction.

J Thorac Dis 2020 Aug;12(8):3995-4001

Department of Cardiothoracic Surgery, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Background: An isolated cervical or thoracic surgical approach provides insufficient exposure for achieving complete resection of tumors of the cervicothoracic junction. This study examines reverse "L" thoracotomy as a surgical approach to these tumors. Additionally, the feasibility, safety, and effectiveness of reverse "L" surgical incision for tumor resection was also analyzed.

Methods: Patients with cervicothoracic tumors were identified from an internal database. Subjects were selected on the basis of undergoing reverse "L" thoracotomy from August 2014 to August 2018. The tumor characteristics, surgical technique, completeness of resection, morbidity, and patient outcome were reviewed.

Results: All patients successfully underwent resection through reverse "L" surgical approach. No patients needed to undergo full sternotomy. There were 6 neurogenic tumors, 4 thyroid adenocarcinomas, 4 bronchogenic tumors, and 7 other cases in the study. The median operative time was 191.0 min (range, 113.0-348.0 min) and postoperative in-hospital stay ranged from 3 to 7 days. Horner syndrome was observed in 1 case. Hoarseness and lymphatic leakage were evident in 3 and 1 case(s), respectively. Hemidiaphragm paralysis was observed in 1 case. Three cases were unsuccessful in achieving R0 resection. The duration of follow-up ranged from 6 to 42 months. Eleven of 13 patients who underwent resection had no evidence of tumor recurrence. Two patients with metastatic disease died of distant progression within 15 months.

Conclusions: Applying reverse "L" surgical approach is safe, feasible, and effective for the resection of giant tumors of the cervicothoracic junction.
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http://dx.doi.org/10.21037/jtd-20-288BDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7475594PMC
August 2020

High hsa_circ_0020123 expression indicates poor progression to non-small cell lung cancer by regulating the miR-495/HOXC9 axis.

Aging (Albany NY) 2020 Sep 14;12(17):17343-17352. Epub 2020 Sep 14.

Department of Cardiothoracic Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, China.

Circular RNAs (circRNAs) belong to non-protein-coding RNAs that regulate different pathophysiological procedures. Upregulation of hsa_circ_0020123 is found in non-small cell lung cancer (NSCLC); however, its activity and functions are not clear. In this study, the results showed that hsa_circ_0020123 expression increased in both tumor tissues and NSCLC cells. A higher hsa_circ_0020123 expression also led to poor prognoses among NSCLC patients assayed via FISH. The data of FISH also confirmed that hsa_circ_0020123 primarily had a cytoplasmic location. Hsa_circ_0020123 knockdown caused a significant decrease in nude mouse xenograft growth. Bioinformatics analyses and dual luciferase reporter assays confirmed that hsa_circ_0020123 was an miR-495 sponge and that the gene was a miR-495 target. The miR-495 downregulation reversed cell migration and proliferation inhibition induced by hsa_circ_0020123 silencing . HOXC9 overexpression reversed miR-495-induced inhibition of cell migration and proliferation. The dual luciferase reporter assay demonstrated that hsa_circ_0020123 interacted with miR-495 by binding to the HOXC9 3'-UTR to suppresses post-transcriptional HOXC9 expression. Taken together, our study found that hsa_circ_0020123 functioned like a tumor promoter via a novel hsa_circ_0020123/miR-495/HOXC9 axis, highlighting its possibility as a new NSCLC therapeutic target.
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http://dx.doi.org/10.18632/aging.103722DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7521531PMC
September 2020

HAX1 enhances the survival and metastasis of non-small cell lung cancer through the AKT/mTOR and MDM2/p53 signaling pathway.

Thorac Cancer 2020 11 14;11(11):3155-3167. Epub 2020 Sep 14.

Department of Thoracic Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China.

Background: HS-1-associated protein-1 (HAX1) has been reported to be overexpressed in non-small cell lung cancer (NSCLC) tissues. However, the underlying mechanism of HAX1 in NSCLC has not previously been demonstrated. The present study investigated the role and underlying mechanism of HAX1 in NSCLC.

Methods: The HAX1 expression were confirmed in NSCLC tissues through TCGA database and qRT-PCR. Moreover, we performed qRT-PCR, Western blotting, Transwell assays, TUNEL assays and so on to evaluate the role of HAX1 in A549 and H1299 cell lines.

Results: mRNA expression of HAX1 was overexpressed in NSCLC tissues compared to adjacent normal tissues according to The Cancer Genome Atlas (TCGA) database. QRT-PCR assays showed that HAX1 mRNA expression was upregulated in NSCLC tissues. The high HAX1 mRNA levels were found to be positively associated with tumor size, TNM stage and lymphatic metastasis. Silencing of HAX1 promoted apoptosis and reduced invasion of A549 and H1299 cells by inhibiting the AKT/mTOR and MDM2/P53 signal pathway. AKT agonist SC79 could inhibit apoptosis and promote proliferation, migration and invasion of A549 and H1299 cells transfected with si-HAX1.

Conclusions: The present study provided a better understanding of HAX1 mechanism in NSCLC and potential therapeutic target for NSCLC.
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http://dx.doi.org/10.1111/1759-7714.13634DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7606027PMC
November 2020

The CRL3 E3 ubiquitin ligase complex targets TNFAIP1 for degradation to suppress cancer cell migration.

Signal Transduct Target Ther 2020 04 24;5(1):42. Epub 2020 Apr 24.

Cancer Institute, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.

Tumor necrosis factor alpha-induced protein 1 (TNFAIP1) modulates a plethora of important biological processes, including tumorigenesis and cancer cell migration. However, the regulatory mechanism of TNFAIP1 degradation remains largely elusive. In the present study, with a label-free quantitative proteomic approach, TNFAIP1 was identified as a novel ubiquitin target of the Cullin-RING E3 ubiquitin ligase (CRL) complex. More importantly, Cul3-ROC1 (CRL3), a subfamily of CRLs, was identified to specifically interact with TNFAIP1 and promote its polyubiquitination and degradation. Mechanistically, BTBD9, a specific adaptor component of CRL3 complex, was further defined to bind and promote the ubiquitination and degradation of TNFAIP1 in cells. As such, downregulation of BTBD9 promoted lung cancer cell migration by upregulating the expression of TNFAIP1, whereas TNFAIP1 deletion abrogated this effect. Finally, bioinformatics and clinical sample analyses revealed that BTBD9 was downregulated while TNFAIP1 was overexpressed in human lung cancer, which was associated with poor overall survival of patients. Taken together, these findings reveal a previously unrecognized mechanism by which the CRL3 ubiquitin ligase controls TNFAIP1 degradation to regulate cancer cell migration.
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http://dx.doi.org/10.1038/s41392-020-0140-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7181851PMC
April 2020

GLUT5-mediated fructose utilization drives lung cancer growth by stimulating fatty acid synthesis and AMPK/mTORC1 signaling.

JCI Insight 2020 02 13;5(3). Epub 2020 Feb 13.

Cancer Institute, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.

Lung cancer (LC) is a leading cause of cancer-related deaths worldwide. Its rapid growth requires hyperactive catabolism of principal metabolic fuels. It is unclear whether fructose, an abundant sugar in current diets, is essential for LC. We demonstrated that, under the condition of coexistence of metabolic fuels in the body, fructose was readily used by LC cells in vivo as a glucose alternative via upregulating GLUT5, a major fructose transporter encoded by solute carrier family 2 member 5 (SLC2A5). Metabolomic profiling coupled with isotope tracing demonstrated that incorporated fructose was catabolized to fuel fatty acid synthesis and palmitoleic acid generation in particular to expedite LC growth in vivo. Both in vitro and in vivo supplement of palmitoleic acid could restore impaired LC propagation caused by SLC2A5 deletion. Furthermore, molecular mechanism investigation revealed that GLUT5-mediated fructose utilization was required to suppress AMPK and consequently activate mTORC1 activity to promote LC growth. As such, pharmacological blockade of in vivo fructose utilization using a GLUT5 inhibitor remarkably curtailed LC growth. Together, this study underscores the importance of in vivo fructose utilization mediated by GLUT5 in governing LC growth and highlights a promising strategy to treat LC by targeting GLUT5 to eliminate those fructose-addicted neoplastic cells.
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http://dx.doi.org/10.1172/jci.insight.131596DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7098789PMC
February 2020

Effective targeting of the ubiquitin-like modifier NEDD8 for lung adenocarcinoma treatment.

Cell Biol Toxicol 2020 08 6;36(4):349-364. Epub 2020 Jan 6.

Cancer Institute, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200032, China.

Protein neddylation, a process of conjugating neural precursor cell expressed, developmentally downregulated 8 (NEDD8) to substrates, plays a tumor-promoting role in lung carcinogenesis. Our previous study showed MLN4924, an inhibitor of NEDD8 activating enzyme (E1), significantly inhibits the growth of multiple cancer cells. However, resistance can develop to MLN4924 by mutation. Therefore, it is important to further understand how NEDD8 acts in lung cancer. In the present study, we demonstrated NEDD8 is overactivated in lung cancers and confers a worse patient overall survival. Furthermore, we report that in lung adenocarcinoma cells, NEDD8 depletion significantly suppressed lung cancer cell growth and progression both in vitro and in vivo. Mechanistic studies revealed that NEDD8 depletion induced the accumulation of a panel of tumor-suppressive cullin-RING ubiquitin ligase substrates (e.g., p21, p27, and Wee1) via blocking their degradation, triggering cell cycle arrest at G phase, thus inducing apoptosis or senescence in a cell-line-dependent manner. The present study demonstrates the role of NEDD8 in regulating the malignant phenotypes of lung cancer cells and further validates NEDD8 as a potential therapeutic target in lung cancer.
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http://dx.doi.org/10.1007/s10565-019-09503-6DOI Listing
August 2020

Optical nanomanipulation on solid substrates via optothermally-gated photon nudging.

Nat Commun 2019 12 12;10(1):5672. Epub 2019 Dec 12.

Materials Science and Engineering Program and Texas Materials Institute, The University of Texas at Austin, Austin, TX, USA.

Constructing colloidal particles into functional nanostructures, materials, and devices is a promising yet challenging direction. Many optical techniques have been developed to trap, manipulate, assemble, and print colloidal particles from aqueous solutions into desired configurations on solid substrates. However, these techniques operated in liquid environments generally suffer from pattern collapses, Brownian motion, and challenges that come with reconfigurable assembly. Here, we develop an all-optical technique, termed optothermally-gated photon nudging (OPN), for the versatile manipulation and dynamic patterning of a variety of colloidal particles on a solid substrate at nanoscale accuracy. OPN takes advantage of a thin surfactant layer to optothermally modulate the particle-substrate interaction, which enables the manipulation of colloidal particles on solid substrates with optical scattering force. Along with in situ optical spectroscopy, our non-invasive and contactless nanomanipulation technique will find various applications in nanofabrication, nanophotonics, nanoelectronics, and colloidal sciences.
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http://dx.doi.org/10.1038/s41467-019-13676-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6908671PMC
December 2019

ARHGAP24 inhibits cell proliferation and cell cycle progression and induces apoptosis of lung cancer via a STAT6-WWP2-p27 axis.

Carcinogenesis 2020 07;41(5):711-721

Department of Cardiothoracic Surgery, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Rho GTPase-activating proteins (RhoGAPs) have been reported to be of great importance in the initiation and development of many different cancers. However, their biological roles and regulatory mechanisms in lung cancer development and progression are poorly defined. Real-time PCR or western blotting analysis was used to detect Rho GTPase-activating protein 24 (ARHGAP24), WWP2, p27, p-STAT6 and STAT6 expression levels as well as the activity of RhoA and Rac1 in lung cancer. Cell proliferation, apoptosis and cell cycle were measured by CCK-8 and flow cytometry analysis. Tumor growth of lung cancer cells was measured using a nude mouse xenograft experiment model in vivo. The correlation between WWP2 and p27 was measured by co-immunoprecipitation and ubiquitination analysis. We found that ARHGAP24 expression was lower in lung cancer tissues collected from the The Cancer Genome Atlas and independent hospital database. Overexpression of ARHGAP24 significantly suppressed cell proliferation and the activity of RhoA and Rac1, induced cell apoptosis and arrested cell cycle at the G0-G1 phase. ARHGAP24 overexpression also inhibited tumor growth in nude mice, whereas knockdown of ARHGAP24 significantly promoted cell proliferation and WWP2 expression and inhibited cell cycle arrest at G1 phase through activating STAT6 signaling. ARHGAP24 overexpression inhibited WWP2 overexpression-induced cell proliferation, cell cycle progression and the decreased p27 expression. Moreover, WWP2 was found interacted with p27, and WWP2 overexpression promoted the ubiquitination of p27. In conclusion, our findings suggest that ARHGAP24 inhibits cell proliferation and cell cycle progression and induces cell apoptosis of lung cancer via a STAT6-WWP2-p27 axis.
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http://dx.doi.org/10.1093/carcin/bgz144DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7197742PMC
July 2020

Validation of NEDD8-conjugating enzyme UBC12 as a new therapeutic target in lung cancer.

EBioMedicine 2019 Jul 14;45:81-91. Epub 2019 Jun 14.

Cancer Institute of Traditional Chinese Medicine, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Electronic address:

Background: The neddylation pathway is overactivated in human cancers. Inhibition of neddylation pathway has emerged as an attractive anticancer strategy. The mechanisms underlying neddylation overactivation in cancer remain elusive. MLN4924/Pevonedistat, a first-in-class NEDD8-activating enzyme (NAE, E1) inhibitor, exerts significant anti-tumor effects, but its mutagenic resistance remains unresolved.

Methods: The expression of NEDD8-conjugating enzyme UBC12/UBE2M (E2) and NEDD8 were estimated by bioinformatics analysis and western blot in human lung cancer cell lines. The malignant phenotypes of lung cancer cells were evaluated both in vitro and in vivo upon UBC12 knockdown. Cell-cycle arrest was evaluated by quantitative proteomic analysis and propidium iodide stain and fluorescence - activated cell sorting (FACS). The growth of MLN4924 - resistant H1299 cells was also evaluated upon UBC12 knockdown.

Findings: The mRNA level of UBC12 in lung cancer tissues was much higher than that in normal lung tissues, increased with disease deterioration, and positively correlated with NEDD8 expression. Moreover, the overexpression of UBC12 significantly enhanced protein neddylation modification whereas the downregulation of UBC12 reduced neddylation modification of target proteins. Functionally, neddylation inactivation by UBC12 knockdown suppressed the malignant phenotypes of lung cancer cells both in vitro and in vivo. The quantitative proteomic analysis and cell cycle profiling showed that UBC12 knockdown disturbed cell cycle progression by triggering G phase cell-cycle arrest. Further mechanistical studies revealed that UBC12 knockdown inhibited Cullin neddylation, led to the inactivation of CRL E3 ligases and induced the accumulation of tumor-suppressive CRL substrates (p21, p27 and Wee1) to induce cell cycle arrest and suppress the malignant phenotypes of lung cancer cells. Finally, UBC12 knockdown effectively inhibited the growth of MLN4924-resistant lung cancer cells.

Interpretation: These findings highlight a crucial role of UBC12 in fine-tuned regulation of neddylation activation status and validate UBC12 as an attractive alternative anticancer target against neddylation pathway. FUND: Chinese Minister of Science and Technology grant (2016YFA0501800), National Natural Science Foundation of China (Grant Nos. 81401893, 81625018, 81820108022, 81772470, 81572340 and 81602072), Innovation Program of Shanghai Municipal Education Commission (2019-01-07-00-10-E00056), Program of Shanghai Academic/Technology Research Leader (18XD1403800), National Thirteenth Five-Year Science and Technology Major Special Project for New Drug and Development (2017ZX09304001). The funders had no role in study design, data collection, data analysis, interpretation, writing of the report.
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http://dx.doi.org/10.1016/j.ebiom.2019.06.005DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6642072PMC
July 2019

Dark-Exciton-Mediated Fano Resonance from a Single Gold Nanostructure on Monolayer WS at Room Temperature.

Small 2019 Aug 11;15(31):e1900982. Epub 2019 Jun 11.

Department of Mechanical Engineering, Texas Materials Institute, The University of Texas at Austin, Austin, TX, 78712, USA.

Strong spatial confinement and highly reduced dielectric screening provide monolayer transition metal dichalcogenides with strong many-body effects, thereby possessing optically forbidden excitonic states (i.e., dark excitons) at room temperature. Herein, the interaction of surface plasmons with dark excitons in hybrid systems consisting of stacked gold nanotriangles and monolayer WS is explored. A narrow Fano resonance is observed when the hybrid system is surrounded by water, and the narrowing of the spectral Fano linewidth is attributed to the plasmon-enhanced decay of dark K-K excitons. These results reveal that dark excitons in monolayer WS can strongly modify Fano resonances in hybrid plasmon-exciton systems and can be harnessed for novel optical sensors and active nanophotonic devices.
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http://dx.doi.org/10.1002/smll.201900982DOI Listing
August 2019

Mitochondrial NDUFA4L2 protein promotes the vitality of lung cancer cells by repressing oxidative stress.

Thorac Cancer 2019 04 2;10(4):676-685. Epub 2019 Feb 2.

Department of Cardiothoracic Surgery, Xin Hua Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Background: Non-small cell lung cancer (NSCLC) accounts for a significant proportion of cancer-related deaths and lacks an effective treatment strategy. NSCLC tissues are generally found in a low oxygen environment. The NDUFA4L2 protein, located in the mitochondria, is encoded by the nucleus genome and is considered a crucial mediator that regulates cell survival. A better understanding of the mechanism of NDUFA4L2 in NSCLC survival in hypoxic environments is essential to design new therapeutic methods.

Methods: Twenty NSCLC and corresponding paired non-tumorous lung tissue samples were collected. NSCLC cell lines were cultured in hypoxic conditions to investigate the mechanism of NDUFA4L2 in NSCLC. The role of NDUFA4L2 was confirmed by using Western blotting, reactive oxygen species measurement, flow cytometry, immunofluorescence analysis, and wound healing and colony formation assays.

Results: The expression of HIF-1α and mitochondrial NDUFA4L2 increased in NSCLC cell lines cultured in hypoxic conditions (1% O ). NDUFA4L2 was drastically overexpressed in human NSCLC tissues and cell lines cultured in hypoxic conditions. HIF-1α regulated the expression of NDUFA4L2. Knockdown of NDUFA4L2 notably increased mitochondrial reactive oxygen species production, which suppressed the viability of NSCLC.

Conclusion: In conclusion, overexpression of NDUFA4L2 is a key factor for maintaining NSCLC growth, suggesting that mitochondrial NDUFA4L2 may be a potential target for the treatment of lung cancer.
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http://dx.doi.org/10.1111/1759-7714.12984DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6449242PMC
April 2019

Rho GTPase Activating Protein 24 (ARHGAP24) Silencing Promotes Lung Cancer Cell Migration and Invasion by Activating β-Catenin Signaling.

Med Sci Monit 2019 Jan 1;25:21-31. Epub 2019 Jan 1.

Department of Cardiothoracic Surgery, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China (mainland).

BACKGROUND Rho GTPase activating protein (RhoGAPs) is an important negative regulator of the Rho signaling pathway that is involved in tumorigenesis in liver, colon, and renal cancer. However, the mechanism by which Rho GTPase activating protein 24 (ARHGAP24) regulates cell invasion and migration of lung cancer has not been fully explained. MATERIAL AND METHODS In this study, ARHGAP24 expression in lung cancer tissues and cell lines was measured by immunohistochemical and Western blot analysis. Transwell or wound healing analysis was performed to detect the cell migration and invasion of ARHGAP24 modulated A549 and NCI-H1975 cells with β-catenin inhibitor XAV-939 (10 µM) treatment, and the expression of MMP9, VEGF, and β-catenin protein was measured by Western blotting. RESULTS Our results showed that ARHGAP24 expression was downregulated in lung cancer tissues and cell lines. pLVX-Puro-ARHGAP24 transfection in A549 cells significantly inhibited cell invasion and migration, along with increased E-cadherin and decreased MMP9, VEGF, Vimentin, and β-catenin protein expression. pLKO.1-ARHGAP24-shRNA transfection in NCI-H1975 cells significantly promoted cell invasion and migration, accompanied with decreased E-cadherin and increased MMP9, VEGF, and β-catenin protein expression. Moreover, NCI-H1975 cells with XAV-939 treatment showed decreased cell invasion and migration when compared with pLKO.1-ARHGAP24-shRNA transfection. ARHGAP24 silencing promoted the transcriptional activity of β-catenin in NCI-H1975 cells. CONCLUSIONS Our findings indicate that ARHGAP24 silencing promotes lung cancer cell migration and invasion through activating β-catenin signaling.
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http://dx.doi.org/10.12659/MSM.911503DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6327779PMC
January 2019

Thoracoscopy Assisted Minimally Surgery (NUSS procedure) for Pectus Excavatum vs. Novel Modified NUSS procedure - A Single-Center Retrospective Study.

Heart Surg Forum 2018 Sep 27;21(5):E404-E408. Epub 2018 Sep 27.

Department of Cardiothoracic Surgery, Xinhua Hospital, Shanghai Jiaotong University. Shanghai, China.

Objective: The purpose of this article is to evaluate the efficacy of thoracoscopy assisted minimally surgery (NUSS procedure) for pectus excavatum and novel modified NUSS procedure by comparing the data of patients of pectus excavatum who had undergone novel modified NUSS Procedure or NUSS procedure.

Methods: A retrospective study was performed, involving 132 cases of patients with pectus excavatum collected from Shanghai Jiaotong University School of Medicine Xinhua Hospital cardio-thoracic surgery between Jan. 2009 and Jan. 2012. The 132 patients were strictly divided into two groups: Group A included 76 cases that underwent a novel modified NUSS procedure; Group B included 56 cases that underwent NUSS procedure. Compared data included gender, age, operative time, blood loss, postoperative hospital staying and clinical variables and demographic were compared with univariable analysis.

Results: No statistically significant correlations were observed in the two groups, such as age (12.67±4.793 years vs. 12.20± 6.423 years), sex, and other clinical data (P > 0.05). In Group A, postoperative hospitalization time (3.95±0.487 days vs. 6.07±1.412 days), operation time (46.28±12.218 minutes vs. 72.23±24.270 minutes), and blood loss (7.37±4.863 ml vs. 16.93±14.002 ml) were significantly better than those in Group B (P < 0.05), shortening hospitalization time, reducing costs, meaning statistically significant differences. There was no recurrence in Group A and Group B after operation.

Conclusion: The study demonstrated that novel modified NUSS procedure is less invasive, having rapid recovery, shortening the time of hospital stay, and reducing hospital cost. Thus, it is safe, worth promoting, and is widely being used.
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http://dx.doi.org/10.1532/hsf.2034DOI Listing
September 2018

Opto-thermoelectric nanotweezers.

Nat Photonics 2018 Apr 26;12(4):195-201. Epub 2018 Mar 26.

Department of Mechanical Engineering, The University of Texas at Austin, Austin, TX 78712, USA.

Optical manipulation of plasmonic nanoparticles provides opportunities for fundamental and technical innovation in nanophotonics. Optical heating arising from the photon-to-phonon conversion is considered as an intrinsic loss in metal nanoparticles, which limits their applications. We show here that this drawback can be turned into an advantage, by developing an extremely low-power optical tweezing technique, termed opto-thermoelectric nanotweezers (OTENT). Through optically heating a thermoplasmonic substrate, alight-directed thermoelectric field can be generated due to spatial separation of dissolved ions within the heating laser spot, which allows us to manipulate metal nanoparticles of a wide range of materials, sizes and shapes with single-particle resolution. In combination with dark-field optical imaging, nanoparticles can be selectively trapped and their spectroscopic response can be resolved . With its simple optics, versatile low-power operation, applicability to diverse nanoparticles, and tuneable working wavelength, OTENT will become a powerful tool in colloid science and nanotechnology.
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http://dx.doi.org/10.1038/s41566-018-0134-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5958900PMC
April 2018

High-Performance Ultrathin Active Chiral Metamaterials.

ACS Nano 2018 05 3;12(5):5030-5041. Epub 2018 May 3.

Department of Mechanical Engineering, Materials Science and Engineering Program, and Texas Materials Institute , The University of Texas at Austin , Austin , Texas 78712 , United States.

Ultrathin active chiral metamaterials with dynamically tunable and responsive optical chirality enable new optical sensors, modulators, and switches. Herein, we develop ultrathin active chiral metamaterials of highly tunable chiroptical responses by inducing tunable near-field coupling in the metamaterials and exploit the metamaterials as ultrasensitive sensors to detect trace amounts of solvent impurities. To demonstrate the active chiral metamaterials mediated by tunable near-field coupling, we design moiré chiral metamaterials (MCMs) as model metamaterials, which consist of two layers of identical Au nanohole arrays stacked upon one another in moiré patterns with a dielectric spacer layer between the Au layers. Our simulations, analytical fittings, and experiments reveal that spacer-dependent near-field coupling exists in the MCMs, which significantly enhances the spectral shift and line shape change of the circular dichroism (CD) spectra of the MCMs. Furthermore, we use a silk fibroin thin film as the spacer layer in the MCM. With the solvent-controllable swelling of the silk fibroin thin films, we demonstrate actively tunable near-field coupling and chiroptical responses of the silk-MCMs. Impressively, we have achieved the spectral shift over a wavelength range that is more than one full width at half-maximum and the sign inversion of the CD spectra in a single ultrathin (1/5 of wavelength in thickness) MCM. Finally, we apply the silk-MCMs as ultrasensitive sensors to detect trace amounts of solvent impurities down to 200 ppm, corresponding to an ultrahigh sensitivity of >10 nm/refractive index unit (RIU) and a figure of merit of 10/RIU.
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http://dx.doi.org/10.1021/acsnano.8b02566DOI Listing
May 2018

Tunable Fano Resonance and Plasmon-Exciton Coupling in Single Au Nanotriangles on Monolayer WS at Room Temperature.

Adv Mater 2018 May 16;30(22):e1705779. Epub 2018 Apr 16.

Department of Mechanical Engineering, Materials Science and Engineering Program, Texas Materials Institute, The University of Texas at Austin, Austin, TX, 78712, USA.

Tunable Fano resonances and plasmon-exciton coupling are demonstrated at room temperature in hybrid systems consisting of single plasmonic nanoparticles deposited on top of the transition metal dichalcogenide monolayers. By using single Au nanotriangles (AuNTs) on monolayer WS as model systems, Fano resonances are observed from the interference between a discrete exciton band of monolayer WS and a broadband plasmonic mode of single AuNTs. The Fano lineshape depends on the exciton binding energy and the localized surface plasmon resonance strength, which can be tuned by the dielectric constant of surrounding solvents and AuNT size, respectively. Moreover, a transition from weak to strong plasmon-exciton coupling with Rabi splitting energies of 100-340 meV is observed by rationally changing the surrounding solvents. With their tunable plasmon-exciton interactions, the proposed WS -AuNT hybrids can open new pathways to develop active nanophotonic devices.
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http://dx.doi.org/10.1002/adma.201705779DOI Listing
May 2018

Tunable Resonance Coupling in Single Si Nanoparticle-Monolayer WS Structures.

ACS Appl Mater Interfaces 2018 May 3;10(19):16690-16697. Epub 2018 May 3.

Photonics Initiative, Advanced Science Research Center , City University of New York , New York , New York 10031 , United States.

Two-dimensional semiconducting transition metal dichalcogenides (TMDCs) are extremely attractive materials for optoelectronic applications in the visible and near-infrared range. Coupling these materials to optical nanocavities enables advanced quantum optics and nanophotonic devices. Here, we address the issue of resonance coupling in hybrid exciton-polariton structures based on single Si nanoparticles (NPs) coupled to monolayer (1L)-WS. We predict a strong coupling regime with a Rabi splitting energy exceeding 110 meV for a Si NP covered by 1L-WS at the magnetic optical Mie resonance because of the symmetry of the mode. Further, we achieve a large enhancement in the Rabi splitting energy up to 208 meV by changing the surrounding dielectric material from air to water. The prediction is based on the experimental estimation of TMDC dipole moment variation obtained from the measured photoluminescence spectra of 1L-WS in different solvents. An ability of such a system to tune the resonance coupling is realized experimentally for optically resonant spherical Si NPs placed on 1L-WS. The Rabi splitting energy obtained for this scenario increases from 49.6 to 86.6 meV after replacing air by water. Our findings pave the way to develop high-efficiency optoelectronic, nanophotonic, and quantum optical devices.
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http://dx.doi.org/10.1021/acsami.7b17112DOI Listing
May 2018

Cas9-nickase-mediated genome editing corrects hereditary tyrosinemia in rats.

J Biol Chem 2018 05 5;293(18):6883-6892. Epub 2018 Mar 5.

From the Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai 200241, China,

Hereditary tyrosinemia type I (HTI) is a metabolic genetic disorder caused by mutation of fumarylacetoacetate hydrolase (FAH). Because of the accumulation of toxic metabolites, HTI causes severe liver cirrhosis, liver failure, and even hepatocellular carcinoma. HTI is an ideal model for gene therapy, and several strategies have been shown to ameliorate HTI symptoms in animal models. Although CRISPR/Cas9-mediated genome editing is able to correct the mutation in mouse models, WT Cas9 induces numerous undesired mutations that have raised safety concerns for clinical applications. To develop a new method for gene correction with high fidelity, we generated a mutant rat model to investigate whether Cas9 nickase (Cas9n)-mediated genome editing can efficiently correct the First, we confirmed that Cas9n rarely induces indels in both on-target and off-target sites in cell lines. Using WT Cas9 as a positive control, we delivered Cas9n and the repair donor template/single guide (sg)RNA through adenoviral vectors into HTI rats. Analyses of the initial genome editing efficiency indicated that only WT Cas9 but not Cas9n causes indels at the on-target site in the liver tissue. After receiving either Cas9n or WT Cas9-mediated gene correction therapy, HTI rats gained weight steadily and survived. Fah-expressing hepatocytes occupied over 95% of the liver tissue 9 months after the treatment. Moreover, CRISPR/Cas9-mediated gene therapy prevented the progression of liver cirrhosis, a phenotype that could not be recapitulated in the HTI mouse model. These results strongly suggest that Cas9n-mediated genome editing is a valuable and safe gene therapy strategy for this genetic disease.
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http://dx.doi.org/10.1074/jbc.RA117.000347DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5936814PMC
May 2018

Concomitant thoracoscopic surgery for solitary pulmonary nodule and atrial fibrillation.

Interact Cardiovasc Thorac Surg 2018 03;26(3):402-406

Department of Cardiothoracic Surgery, School of Medicine, Xinhua Hospital, Shanghai Jiaotong University, Shanghai, China.

Objectives: The incidence of both solitary pulmonary nodules (SPN) and non-valvular atrial fibrillation (NVAF) has increased over the past decade. We performed concomitant video-assisted thoracoscopic surgery with modified epicardial radiofrequency ablation procedure for NVAF and SPN resection.

Methods: Sixteen patients (7 men, mean age 62.6 ± 11.2 years) with SPN and NVAF underwent this procedure. Of these patients, 10 had paroxysmal atrial fibrillation and 6 persistent atrial fibrillation. A modified epicardial radiofrequency ablation combined with pulmonary vein isolation, circumferential left atrial ablation, ganglionic plexus ablation and left atrial appendage resection was performed for all patients. Left pulmonary surgery was carried out subsequently.

Results: The mean procedure duration was 203.1 ± 15.6 (range 177-224) min. All patients successfully underwent this procedure with no conversion to sternotomy or pacemaker implantation. Of the 16 included patients, 13 received lobectomy and 3 received wedge resection. No severe complications occurred postoperatively. The mean length of hospital stay was 9.1 ± 1.4 (range 7-11) days with a mean follow-up period of 18.7 ± 6.7 (range 8-32) months. One patient had AF recurrence 6 months postoperatively. No pulmonary vein stenosis was detected at the 3rd postoperative month. There were no deaths or thromboembolic events during follow-up.

Conclusions: This concomitant therapy proved to be safe and yielded good clinical outcomes. Therefore, it deserves to be considered as a treatment for patients with SPN and NVAF.
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http://dx.doi.org/10.1093/icvts/ivx346DOI Listing
March 2018

Knockdown of SOX12 expression inhibits the proliferation and metastasis of lung cancer cells.

Am J Transl Res 2017 15;9(9):4003-4014. Epub 2017 Sep 15.

Department of Cardiothoracic Surgery, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghai 200092, China.

Sex determining region Y-box protein 12 (SOX12) plays an important role in the tumorigenesis of hepatocellular carcinoma. The involvement of SOX12 in human lung cancer is not well-understood. The aim of the current study was to explore the expression pattern and function of SOX12 in lung cancer. SOX12 expression in lung cancer tissues was elevated as assessed by analyzing The Cancer Genome Atlas (TCGA) lung cancer cohort and real-time PCR data of our own cohort. We found that SOX12 mRNA expression was up-regulated in 83.3% (75/90) of the lung cancer tissues in comparison with paired normal tissues. Moreover, high SOX12 expression predicted reduced overall survival. We also found that knockdown of SOX12 in SPC-A-1 and A549 cells impaired lung cancer cell proliferation, migration and invasion , but promoted lung cancer cell apoptosis. tumorigenesis experiments showed that inhibition of SOX12 expression significantly suppressed the growth of xenograft tumors. Finally, the mRNA and protein levels of cell growth (PCNA and Cyclin E), apoptosis (Bcl-2 and Bax), invasion (matrix metalloproteinase-9) and epithelial-mesenchymal transition (EMT; Twist1 and E-cadherin) related moderators were affected by SOX12 knockdown. Chromatin immunoprecipitation assays showed that Cyclin E and Twist1 were direct transcriptional targets of SOX12. Taken together, our study suggests that SOX12 functions as an oncogenic molecule during the development of human lung cancer.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5622245PMC
September 2017

Controlling Plasmon-Enhanced Fluorescence via Intersystem Crossing in Photoswitchable Molecules.

Small 2017 10 21;13(38). Epub 2017 Aug 21.

Department of Mechanical Engineering, Texas Materials Institute, The University of Texas at Austin, Austin, TX, 78712, USA.

By harnessing photoswitchable intersystem crossing (ISC) in spiropyran (SP) molecules, active control of plasmon-enhanced fluorescence in the hybrid systems of SP molecules and plasmonic nanostructures is achieved. Specifically, SP-derived merocyanine (MC) molecules formed by photochemical ring-opening reaction display efficient ISC due to their zwitterionic character. In contrast, ISC in quinoidal MC molecules formed by thermal ring-opening reaction is negligible. The high ISC rate can improve fluorescence quantum yield of the plasmon-modified spontaneous emission, only when the plasmonic electromagnetic field enhancement is sufficiently high. Along this line, extensive photomodulation of fluorescence is demonstrated by switching the ISC in MC molecules at Au nanoparticle aggregates, where strongly enhanced plasmonic hot spots exist. The ISC-mediated plasmon-enhanced fluorescence represents a new approach toward controlling the spontaneous emission of fluorophores near plasmonic nanostructures, which expands the applications of active molecular plasmonics in information processing, biosensing, and bioimaging.
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http://dx.doi.org/10.1002/smll.201701763DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5866054PMC
October 2017

Plasmon-trion and plasmon-exciton resonance energy transfer from a single plasmonic nanoparticle to monolayer MoS.

Nanoscale 2017 Sep;9(37):13947-13955

Department of Mechanical Engineering, The University of Texas at Austin, Austin, TX 78712, USA.

Resonance energy transfer (RET) from plasmonic metal nanoparticles (NPs) to two-dimensional (2D) materials enhances the performance of 2D optoelectronic devices and sensors. Herein, single-NP scattering spectroscopy is employed to investigate plasmon-trion and plasmon-exciton RET from single Au nanotriangles (AuNTs) to monolayer MoS, at room temperature. The large quantum confinement and reduced dielectric screening in monolayer MoS facilitates efficient RET between single plasmonic metal NPs and the monolayer. Because of the large exciton binding energy of monolayer MoS, charged excitons (i.e., trions) are observed at room temperature, which enable us to study the plasmon-trion interactions under ambient conditions. Tuning of plasmon-trion and plasmon-exciton RET is further achieved by controlling the dielectric constant of the medium surrounding the AuNT-MoS hybrids. Our observation of switchable plasmon-trion and plasmon-exciton RET inspires new applications of the hybrids of 2D materials and metal nanoparticles.
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http://dx.doi.org/10.1039/c7nr03909cDOI Listing
September 2017
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