Publications by authors named "Xue-Mei Wan"

8 Publications

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lncRNA Promotes Metastasis of Non-Small Cell Lung Cancer Through EZH2-Mediated Activation of Hippo/NOTCH1 Signaling Pathways.

Cell J 2021 Apr 1;23(1):21-31. Epub 2021 Mar 1.

Department of Cardiovascular Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, P.R China. Email:

Objective: Although growing evidences have showed that long non-coding RNA (lncRNAs) plasmacytoma variant translocation 1 () plays a critical role in the progression of non-small cell lung cancer (NSCLC), there are still many unsolved mysteries remains to be deeply elucidated. This study aimed to find a new underlying mechanism of in regulating the tumorigenesis and development of NSCLC.

Materials And Methods: In this experimental study, Quantitative reverse transcription polymerase chain reaction (qRTPCR) was used to profile the expression of in NSCLC tissues and cells. The effects of on cell growth, migration and invasion were detected by colony formation assay, Matrigel-free transwell and Matrigel transwell assays, respectively. Changes of the key protein expression in Hippo and NOTCH signaling pathways, as well as epithelialmesenchymal transition (EMT) markers, were analyzed using western blot. Interaction of with enhancer of zeste homolog 2 (EZH2) was verified by RNA pull-down, and their binding to the downstream targets was detected by Chromatin Immunoprecipitation (ChIP) assays.

Results: These results showed that was up-regulated in NSCLC tissue and cell lines, promoting NSCLC cell proliferation, migration and invasion. Knockdown of inhibited the expression of Yes-associated protein 1 (YAP1) and NOTCH1 signaling activation. Further, we have confirmed that regulated expression of YAP1 through EZH2-mediated promoter methylation resulting in the inhibition of transcription and its target YAP1 upregulation, and finally NOTCH signaling pathway was activated, which promoted EMT and invasion and metastasis.

Conclusion: These results suggested that lncRNA promotes NSCLC metastasis through EZH2-mediated activation of Hippo/NOTCH1 signaling pathways. This study provides a new opportunity to advance our understanding in the potential mechanism of NSCLC development.
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http://dx.doi.org/10.22074/cellj.2021.7010DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7944120PMC
April 2021

Puerarin induces Nrf2 as a cytoprotective mechanism to prevent cadmium-induced autophagy inhibition and NLRP3 inflammasome activation in AML12 hepatic cells.

J Inorg Biochem 2021 Apr 11;217:111389. Epub 2021 Feb 11.

Hospital of Chengdu University of Traditional Chinese Medicine, No. 39 Shi-er-qiao Road, Chengdu, Sichuan 610072,China. Electronic address:

Liver is the main target organ of cadmium (Cd) toxicity and puerarin (PU) has been shown to prevent Cd-induced hepatic cell damage via its antioxidant activity. Nrf2 acts as a critical regulator of cellular defense against various oxidative insults, but its role in the protection of PU against Cd-induced hepatic damage has not yet been clarified. Hereby, this study was designed to investigate the underlying mechanism using mouse hepatocyte line AML-12. Data firstly showed that Cd-inhibited Nrf2 pathway was markedly restored by PU treatment, assessed by Nrf2 nuclear translocation, protein levels of Keap1 and Nrf2 downstream target genes. Accordingly, Cd-reduced protein levels of antioxidant enzymes were significantly up-regulated by PU. Next, Nrf2 silencing cellular model was established to further elucidate the role of Nrf2 in the protection of PU against Cd-induced hepatic damage. Attenuation of Cd-induced autophagy inhibition and autophagosome accumulation by PU was remarkably countered by Nrf2 silencing. Moreover, alleviation of Cd-induced NLRP3 inflammasome activation by PU was distinctly prevented by Nrf2 knockdown, assessed by protein levels of NLRP3 inflammosome complex and downstream IL-18 and IL-1β production. Collectively, our data suggest that PU restores Cd-induced Nrf2 inhibition to prevent autophagy inhibition and NLRP3 inflammasome activation, providing novel insights into the protection of PU against Cd-induced hepatic cell damage.
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http://dx.doi.org/10.1016/j.jinorgbio.2021.111389DOI Listing
April 2021

Notch1 protects against myocardial ischaemia-reperfusion injury via regulating mitochondrial fusion and function.

J Cell Mol Med 2020 03 23;24(5):3183-3191. Epub 2020 Jan 23.

Department of Cardiovascular Surgery, The First Affiliated Hospital, Nanchang University, Nanchang, 330006, China.

Mitochondrial fusion and fission dynamic are critical to the myocardial protection against ischaemia-reperfusion injury. Notch1 signalling plays an important role in heart development, maturation and repair. However, the role of Notch1 in the myocardial mitochondrial fusion and fission dynamic remains elusive. Here, we isolated myocardial cells from rats and established myocardial ischaemia-reperfusion injury (IRI) model. We modulated Notch1, MFN1 and DRP1 expression levels in myocardial cells via infection with recombinant adenoviruses. The results showed that Notch1 improves the cell viability and mitochondrial fusion in myocardiocytes exposed to IRI. These improvements were dependent on the regulation of MFN1 and DRP1. On the mechanism, we found that MNF1 is transcriptionally activated by RBP-Jk in myocardiocytes. Notch1 also improves the mitochondrial membrane potential in myocardiocytes exposed to IRI. Moreover, we further confirmed the protection of the Notch1-MFN1/Drp1 axis on the post-ischaemic recovery of myocardial performance is associated with the preservation of the mitochondrial structure. In conclusion, this study presented a detailed mechanism by which Notch1 signalling improves mitochondrial fusion during myocardial protection.
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http://dx.doi.org/10.1111/jcmm.14992DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7077547PMC
March 2020

ATG13 restricts viral replication by induction of type I interferon.

J Cell Mol Med 2019 09 3;23(9):6508-6511. Epub 2019 Jul 3.

College of Life Science and Engineering, Center for Biomedical Research, Northwest Minzu University, Lanzhou, China.

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http://dx.doi.org/10.1111/jcmm.14483DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6714170PMC
September 2019

Puerarin prevents cadmium-induced hepatic cell damage by suppressing apoptosis and restoring autophagic flux.

Biomed Pharmacother 2019 Jul 3;115:108929. Epub 2019 May 3.

Hospital of Chengdu University of Traditional Chinese Medicine, No. 39 Shi-er-qiao Road, Chengdu, 610072, Sichuan Province, PR China; Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 611130, PR China. Electronic address:

Cadmium (Cd) is a common heavy metal contamination that is highly toxic to liver. Puerarin (PU), a potent free radical scavenger, has been shown to exert cytoprotective effect in numerous pathological processes. However, whether PU affords protection against Cd-induced hepatotoxicity remains unclear to be known. Here, we aimed to investigate the protective effect of PU on Cd-induced hepatotoxicity in an immortalized mouse hepatocyte line, AML-12. First, Cd-induced cytotoxicity in AML-12 cells was obviously ameliorated by PU treatment. Also, Cd-induced apoptotic cell death was markedly alleviated by PU treatment, evidenced by two methods. Simultaneously, Cd-elevated malondialdehyde and reactive oxygen species levels were significantly reduced by PU administration, demonstrating the antioxidant effect of PU against Cd exposure. Moreover, Cd-induced blockage of autophagic flux in AML-12 cells was obviously restored by PU treatment, evidenced by immunoblot analysis of autophagy marker proteins and tandem fluorescent-tagged LC3 method. Resultantly, Cd-induced autophagosome accumulation was significantly alleviated by PU treatment. In conclusion, these observations demonstrate that PU treatment alleviates Cd-induced hepatic cell damage by inhibiting apoptosis and restoring autophagy activity, which is intimately related with its antioxidant activity.
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http://dx.doi.org/10.1016/j.biopha.2019.108929DOI Listing
July 2019

RETRACTED: Function of the PLZF gene in early development and self-renewal of T cells in mice.

Biochem Biophys Res Commun 2019 04 8;511(4):935-940. Epub 2019 Mar 8.

Center for Biomedical Research, College of Life Science and Engineering, Northwest Minzu University, Lanzhou, 730030, China; State Key Laboratory of Veterinary Etiological Biology, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, 730046, China.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal).. This article has been retracted at the request of < the Editor in Chief. The Editor in Chief has been made aware of numerous problems with this paper regarding authorship, poor or insufficient supervision of researchers and the unauthorized use of data acquired from a lab visit by one of the authors.
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http://dx.doi.org/10.1016/j.bbrc.2019.02.156DOI Listing
April 2019

In Vitro, in Vivo, and Interaction Studies of Nematophagous Fungus Arthrobotrys thaumasia ( Monacrosporium thaumasium) with the Larvae of Trichostrongylides of Sheep.

J Parasitol 2017 12 27;103(6):692-698. Epub 2017 Sep 27.

College of Life Science and Engineering, Northwest University for Nationalities, Lanzhou 730030, China.

It is important to isolate potential candidates from the local isolates of nematophagous fungi and to investigate interaction between the fungal strains and gastrointestinal nematodes for the biological control of parasitic nematodes in livestock. In the present study, we assessed the in vitro predatory activity and the viability of isolates of Arthrobotrys thaumasia ( Monacrosporium thaumasium) after passage through the gastrointestinal tract of sheep. The predatory process of a representative isolate selected against the larvae of trichostrongylids was prepared with a scanning electron microscope (SEM). In vitro experiments tested the ability of 9 native isolates of A. thaumasia to prey on larvae of feces of sheep infected with natural mixed nematodes ( Haemonchus contortus, Trichostongylus colubriformis, Marshallagia mongolica). These isolates of A. thaumasia decreased infectivity of third stage infective larvae (L3) by 75.54-99.97%; 7 isolates decreased infectivity by more than 90%. In vivo experiments also demonstrated significant reductions of L3 numbers in the feces treated with the 9 isolates after passing through the gastrointestinal tract of sheep, and these decreases ranged from 51.68 to 88.16%. The isolates tested were re-isolated in 5-g sub-samples of feces from sheep in each treatment group, indicating that these isolates had the capacity to prey upon larvae of trichostrongylids after the passage through gastrointestinal tract. SEM shows that at 6 hr after the larvae were added, including the second stage larvae (L2) and L3 of trichostrongylids, the isolate NBS 005 caught them; at 8 hr after being caught L2 was penetrated by the fungus while penetration of L3 occurred at 12 hr; at 78 hr post-capture L2 was completely destroyed by the fungus while complete digestion of L3 occurred at 84 hr.
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http://dx.doi.org/10.1645/16-146DOI Listing
December 2017

[Using 9-color Flow Cytometry Immunophenotyping to Detect Activation and Apoptosis of Human TCR Vβ Lymphocyte Subpopulations in Peripheral Blood Samples].

Sichuan Da Xue Xue Bao Yi Xue Ban 2016 Mar;47(2):262-6

Objective: To establish an assay using 9-color flow cytometry immunophenotyping to detect activation and apoptosis of human TCR Vβ lymphocyte subpopulations in peripheral blood samples.

Methods: We used 5 antibodies (CD3, CD4, CD8, CD95, CD69), phospholipids binding proteins Annexin V, TCR Vβ Repertoire Kit and nucleus dye DAPI to establish a 9-color flow cytometry assay. Peripheral blood samples were taken from eight healthy people for test of antibodies and determination of optimal PMT and staining method (single-stained vs stained with all but one antibody).

Results: Appropriate detecting voltage, antibody concentration and compensation methods were determined. The distribution of TCR Vβ subgroup in our samples was consistent with the TCR Vβ Repertoire Kit instruction and other published literature.

Conclusion: We have established a effective easy using 9-color flow cytometry immunophenotyping to detect human TCR Vβ lymphocyte subpopulations in peripheral blood samples.
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March 2016