Publications by authors named "Kui Su"

8 Publications

  • Page 1 of 1

TRAIL-Armed ER Nanosomes Induce Drastically Enhanced Apoptosis in Resistant Tumor in Combination with the Antagonist of IAPs (AZD5582).

Adv Healthc Mater 2021 06 8;10(11):e2100030. Epub 2021 May 8.

School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, 51006, China.

Although mesenchymal stem cells (MSCs) can be engineered to deliver the TNF-related apoptosis-inducing ligand (TRAIL) as an effective anticancer therapy, the clinical application is hampered by the costly manufacturing of therapeutic MSCs. Therefore, it is needed to find an alternative cell-free therapy. In this study, TRAIL-armed endoplasmic reticulum (ER)-derived nanosomes (ERN-T) are successfully prepared with an average size of 70.6 nm in diameter from TRAIL transduced MSCs. It is demonstrated that the ERN-T is significantly more efficient for cancer cell killing than the soluble recombinant TRAIL (rTRAIL). AZD5582 is an antagonist of the inhibitors of apoptosis proteins (IAPs), and its combination with ERN-T induces strikingly enhanced apoptosis in cancerous but not normal cells. AZD5582 sensitizes resistant cancer cells to TRAIL through concomitant downregulation of IAP members like XIAP and the Bcl2 family member Mcl-1. Intravenously infused ERN-Ts accumulate in tumors for over 48 h indicating good tumor tropism and retention. The combination of ERN-T and AZD5582 drastically promotes therapeutic efficacy comparing with the cotreatment by rTRAIL and AZD5582 in a subcutaneous MDA-MB-231 xenograft tumor model. The data thus demonstrate that ERN-T can be a novel cell-free alternative to TRAIL-expressing MSC-based anticancer therapy and its efficacy can be drastically enhanced through combination with AZD5582.
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http://dx.doi.org/10.1002/adhm.202100030DOI Listing
June 2021

Extracellular Vesicle Delivery of TRAIL Eradicates Resistant Tumor Growth in Combination with CDK Inhibition by Dinaciclib.

Cancers (Basel) 2020 May 4;12(5). Epub 2020 May 4.

Institute of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou 51006, China.

Tumour necrosis factor (TNF)-related apoptosis inducing ligand (TRAIL) is a promising anti-cancer agent that rapidly induces apoptosis in cancer cells. Unfortunately, the clinical application of recombinant TRAIL (rTRAIL) has been hampered by its common cancer resistance. Naturally TRAIL is delivered as a membrane-bound form by extracellular vesicles (EV-T) and is highly efficient for apoptosis induction. SCH727965 (dinaciclib), a potent cyclin-dependent kinase (CDK) inhibitor, was shown to synergize with other drugs to get better efficacy. However, it has never been investigated if dinaciclib coordinates with EV-T to enhance therapeutic results. This study explores the potential of combination therapy with EV-T and dinaciclib for cancer treatment. EV-T was successfully derived from human TRAIL transduced cells and shown to partially overcome resistance of A549 cells. Dinaciclib was shown to drastically enhance EV-T killing effects on cancer lines that express good levels of death receptor (DR) 5, which are associated with suppression of CDK1, CDK9 and anti-apoptotic proteins. Combination therapy with low doses of EV-T and dinaciclib induced strikingly enhanced apoptosis and led to complete regression in A549 tumors without any adverse side effects observed in a subcutaneous xenograft model. Tumor infiltration of mass NK cells and macrophages was also observed. These observations thus indicate that the combination of EV-T with dinaciclib is a potential novel therapy for highly effective and safe cancer treatment.
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http://dx.doi.org/10.3390/cancers12051157DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7281120PMC
May 2020

LncRNA UCA1/miR-124 axis modulates TGFβ1-induced epithelial-mesenchymal transition and invasion of tongue cancer cells through JAG1/Notch signaling.

J Cell Biochem 2019 06 11;120(6):10495-10504. Epub 2019 Jan 11.

Department of Oral and Maxillofacial Surgery, The Affiliated Zhongshan Hospital, Sun Yat-sen University, Zhongshan, China.

Tongue cancer remains a massive threat to public health due to the high rate of metastasis. Tumor cell epithelial-mesenchymal transition (EMT), which can be induced by transforming growth factor β1 (TGFβ1), has been regarded as a significant contributor to cancer invasion and migration. In our previous study, long noncoding RNA (lncRNA) MALAT1/miR-124/JAG1 axis modulates the growth of tongue cancer. In addition to metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), another lncRNA, urothelial cancer associated 1 (UCA1), can promote EMT and cancer metastasis. In the present study, UCA1 was overexpressed in tongue cancer tissues and cell lines. UCA1 overexpression was correlated to the poorer prognosis of patients with tongue cancer. UCA1 knockdown significantly suppressed TGFβ1-induced tongue cancer cell invasion and EMT by decreasing vimentin and increasing E-cadherin. Regarding the molecular mechanism, UCA1 could directly bind to microRNA-124 (miR-124) and negatively regulate each other. UCA1 knockdown ameliorated, whereas miR-124 inhibition exacerbated TGFβ1-induced EMT and invasion in tongue cancer cells through miR-124 downstream jagged 1 (JAG1) and Notch signaling. Moreover, miR-124 inhibition partially impaired the effect of UCA1 knockdown. In tongue cancer tissues, miR-124 expression was remarkably decreased, whereas JAG1 mRNA expression was increased. miR-124 was negatively correlated with UCA1 and JAG1. UCA1 and JAG1 were positively correlated. In summary, we provided a novel mechanism by which the EMT process and cancer cell invasion in tongue cancer could be modulated from the perspective of lncRNA-miRNA-mRNA regulation.
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http://dx.doi.org/10.1002/jcb.28334DOI Listing
June 2019

[Retracted] Long non‑coding RNA MALAT1 interacts with miR‑124 and modulates tongue cancer growth by targeting JAG1.

Oncol Rep 2018 11 6;40(5):3112. Epub 2018 Sep 6.

Department of Oral and Maxillofacial Surgery, Guanghua School of Stomatology, Hospital of Stomatology, Sun Yat-sen University, Guangzhou, Guangdong 510055, P.R. China.

We wish to retract our research article entitled "Long non‑coding RNA MALAT1 interacts with miR‑124 and modulates tongue cancer growth by targeting JAG1" published in Oncology Reports 37 2087‑2094, 2017. Following the publication of this article, it was drawn to our attention that this paper bore numerous similarites with an article published previously in the journal OncoTargets and Therapy. Although all the data reported in our study were original, we recognize that it was not appropriate that we should have modelled our paper on previously published articles as a template on which to base the writing of our paper. Therefore, we have agreed to follow the Editor's recommendation that this paper be retracted from the publication. All the named authors agree to this retraction. We sincerely apologize to the Editor and the readership of the Journal for our action, and regret any inconvenience this has caused. [the original article was published in the Oncology Reports 37: 2087‑2094, 2017; DOI: 10.3892/or.2017.5445].
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http://dx.doi.org/10.3892/or.2018.6688DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6151889PMC
November 2018

Long non-coding RNA MALAT1 interacts with miR-124 and modulates tongue cancer growth by targeting JAG1.

Oncol Rep 2017 Apr 14;37(4):2087-2094. Epub 2017 Feb 14.

Department of Oral and Maxillofacial Surgery, Guanghua School of Stomatology, Hospital of Stomatology, Sun Yat-sen University, Guangzhou, Guangdong 510055, P.R. China.

Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a long non-coding RNA (lncRNA), was the earliest discovered to be correlated with cancer and contributes to the initiation and development of several types of tumors. Dysregulation of MALAT1 expression is frequently observed in many types of cancer such as gastric cancer, esophageal squamous cell carcinoma and glioma. To date, the role of MALAT1 and the underlying mechanisms in tongue cancer development remain unclear. In the present study, we studied the influence of MALAT1 on tongue cancer cell lines and clinical tongue cancer samples so as to detect its function and the underlying mechanism. In the present study, lncRNA-MALAT1 was specifically upregulated in tongue cancer cell lines and overexpression promoted tongue cancer cell growth by targeting miR-124. Knockdown of MALAT1 suppressed the growth and invasion of human tongue cancer cells and inhibited metastasis in vitro and in vivo. In addition, miR-124-dependent jagged1 (JAG1) regulation was required for MALAT1-induced tongue cancer cell growth. Our data revealed that MALAT1 inhibited tongue cancer cell growth and metastasis through miR-124-dependent JAG1 regulation. In conclusion, we revealed that MALAT1 may play an oncogenic role by increasing proliferation and metastasis of tongue cancer and is a potential therapeutic target in human tongue cancer.
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http://dx.doi.org/10.3892/or.2017.5445DOI Listing
April 2017

TGFβ1-Smad3-Jagged1-Notch1-Slug signaling pathway takes part in tumorigenesis and progress of tongue squamous cell carcinoma.

J Oral Pathol Med 2016 Aug 13;45(7):486-93. Epub 2016 Jan 13.

Department of Oral and Maxillofacial Surgery, Guanghua School of Stomatology, Hospital of Stomatology, Sun Yat-sen University, Guangzhou, Guangdong, China.

Background: TGFβ1 and Smad3 play an important role in the process of EMT. TGFβ1 regulates the expression of Jagged1 by modulating Notch signaling. Jagged1 is related to tumor invasion, metastasis, chemotherapy resistance, and tumor immune escape. The aims of this study are to examine deregulation of TGFβ1-Smad3-Jagged1-Notch1-Slug signaling in TSCC and to investigate its roles in TSCC progression.

Materials And Methods: Notch1, Smad3, Jagged1 and Slug proteins and mRNA expression were detected in specimens from 89 cases of patients. We analyzed the correlation between their expressions and histological grade, clinical stage and lymph node metastasis.

Results: Notch1, Smad3, Jagged1 and Slug mRNA expressions in TSCC were higher than normal tissue (P <0.05). The protein expression of Notch1 and Smad3 in TSCC were higher (χ(2) =7.30, P <0.01 and χ(2) = 5.84, P <0.05). Notch1 and Smad3 expressions were correlated with clinical stage (χ(2) =18.81, P<0.01; χ(2) =22.29, P<0.01), but not Jagged1 (χ(2) =0.53, P>0.05). The Slug protein expression was correlated with clinical stage. The positive rate of Notch1 was higher in lymph node metastases positive cases (χ(2) =7.30, P<0.01). Moreover, higher expression of Jagged1 was found in lymph node positive cases (χ(2) =10.82, P<0.01).

Conclusions: The key protein expression in TGFβ1-Smad3-Jagged1-Notch1-Slug signaling pathway significantly correlated with the clinicopathological features of TSCC patients. It's potential as a biomarker and a novel therapeutic target for TSCC patients at risk of metastasis. It may play an irreplaceable role in TSCC progression which may attribute to promoting EMT which enhances cell migration, invasion and metastasis.
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http://dx.doi.org/10.1111/jop.12406DOI Listing
August 2016

Differences in the effects of filters on health information retrieval from the Internet in three languages from three countries: a comparative study.

Stud Health Technol Inform 2004 ;107(Pt 2):1313-7

Department of Health Management and Informatics, School of Medicine, University of Missouri-Columbia, 62111, USA.

We selected twenty search terms on woman's health from various sources and tested them on Google, once with strict filter on and once with filter off. Searches were specified to three countries (Mainland China, Germany, USA), in three languages (Simplified Chinese, German, US English). We found that the proportion of relevant women's health web sites that were blocked was quite high. For the Chinese language web sites originated in China, 72.6% of the blocked web sites were relevant. For the German language web sites originated in Germany, nearly half (49.4%) were relevant. For the US English web sites originated in the US, 95% were relevant. We concluded that people might unknowingly miss potentially important health information due to information filtering.
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June 2005

How easy/difficult to find information about individual health insurance on the Internet: an examination of ten "quote" web sites.

AMIA Annu Symp Proc 2003 :1022

Department of Health Management and Informatics, School of Medicine, University of Missouri, Columbia, MO, USA.

Ten quote web sites were evaluated to examine the level of difficulty in finding information about individual health insurance. The degrees of ease/difficulty were measured in terms of the number of items to be filled out on the form in order to get a quote. Also examined were whether the quote web sites revealed their identity and whether they provided information about the health plans they quoted. The results showed that some quote web sites did not reveal information about themselves fully. The degrees of ease or difficulty varied from site to site. Not all quote web sites could provide quotes instantly. Among those that provided a quote, the amount of information given on the health plans also varied. Despite the difficulties, the internet has the potential to provide sufficient information.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1480278PMC
December 2004