Knockdown of LncRNA-XIST Suppresses Proliferation and TGF-β1-Induced EMT in NSCLC Through the Notch-1 Pathway by Regulation of miR-137

Wang, Xi; Zhang, Guojun; Cheng, Zhe; Dai, Lingling; Jia, Liting; Jing, Xiaogang; Wang, Huan; Zhang, Rui; Li, Meng; Jiang, Tianci; Yang, Yuan-Jian; Yue, Meng

doi:10.1089/gtmb.2018.0026

Cited by 67 publications

(46 citation statements)

References 32 publications

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“…The present findings clearly demonstrate that the expression of long non-coding RNA (lncRNA XIST) is upregulated in lung cancer cells, and it maybe involve in the cell proliferation and TGF-β1-mediated apoptosis [33]. And lncRNAXIST may have some functions by downregulating miRNA-144.…”

Section: Discussionmentioning

confidence: 52%

LncRNA XIST acts as a microRNA-520 sponge to regulate the cisplatin resistance in NSCLC cells by mediating BAX through ceRNA network

Liu

et al. 2020

Preprint

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Background In recent years, LncRNA acts as a member of competing endogenous RNA (ceRNA), playing an important role in drug resistance of lung cancer. The aim of this study was to identify potential biomarkers about cisplatin resistant lung cancer cells using a comprehensive ceRNA network. Methods GSE6410 (GPL-201) analyzed gene expression changes about cispaltin resistance in A549 NSCLC cells. GSE43249 (GPL-14613) included noncoding RNA expression profiling derived from the cisplatin resistant A549 lung cells. GEO2R, an online analysis tool, analyzed the differentially expressed mRNAs and miRNAs (DEmRNAs and DEmiRNAs). To explore the functional enrichment implication of differentially expressed mRNAs, we used the GO and KEGG pathway analysis. Through miRDB、Targetscan、Starbase、miRWalk, we found targeted miRNAs. The Kaplan-Meier curve method was used to show clinical survival analysis of targeted RNAs (P < 0.05). The Starbase database predicted potential lncRNAs mediated targeted miRNAs. Eventually, the novel ceRNA network of lncRNAs, miRNAs, mRNA was constructed by cytoscape3.7.2. Results 118 differentially expressed mRNAs were the basis of the mediated ceRNA network. DAVID and Kaplan-Meier picked out BAX, an apoptosis regulator. Venn Diagram demonstrated 8 miRNAs commomly regulating Bax. Starbase predicted lncRNA XIST mediated miRNAs. Finally, lncRNA XIST maybe a useful biomarker regulating cisplatin resistance in lung cancer cells. Conclusions LncRNA XIST competitively bound to miRNA 520 in the regulation of cisplatin resistance by BAX, participating apoptosis in the p53 signaling pathway.

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Section: Discussionmentioning

confidence: 52%

LncRNA XIST acts as a microRNA-520 sponge to regulate the cisplatin resistance in NSCLC cells by mediating BAX through ceRNA network

Liu

et al. 2020

Preprint

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show abstract

“…In recent years, lncRNAs have been explored through functional analysis [32]. The present findings clearly demonstrate that the expression of long non-coding RNA (lncRNA XIST) is up-regulated in lung cancer cells, and it maybe involve in the cell proliferation and TGF-β1-mediated apoptosis [33]. And lncRNAXIST may have some functions by downregulating miRNA-144.…”

Section: Discussionmentioning

confidence: 54%

LncRNA XIST acts as a microRNA-520 sponge to regulate the cisplatin resistance in NSCLC cells by mediating BAX through ceRNA network

Liu

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: In recent years, LncRNA acts as a member of competing endogenous RNA (ceRNA), playing an important role in drug resistance of lung cancer. The aim of this study was to identify potential biomarkers about cisplatin resistant lung cancer cells using a comprehensive ceRNA network.Methods: GSE6410 (GPL-201) analyzed gene expression changes about cispaltin resistance in A549 NSCLC cells. GSE43249 (GPL-14613) included noncoding RNA expression profiling derived from the cisplatin resistant A549 lung cells. GEO2R, an online analysis tool, analyzed the differentially expressed mRNAs and miRNAs (DEmRNAs and DEmiRNAs). To explore the functional enrichment implication of differentially expressed mRNAs, we used the GO and KEGG pathway analysis. Through miRDB、Targetscan、Starbase、miRWalk, we found targeted miRNAs. The Kaplan-Meier curve method was used to show clinical survival analysis of targeted RNAs (P<0.05). The Starbase database predicted potential lncRNAs mediated targeted miRNAs. Eventually, the novel ceRNA network of lncRNAs, miRNAs, mRNA was constructed by cytoscape3.7.2.Results:118 differentially expressed mRNAs were the basis of the mediated ceRNA network. DAVID and Kaplan-Meier picked out BAX, an apoptosis regulator. Venn Diagram demonstrated 8 miRNAs commomly regulating Bax. Starbase predicted lncRNA XIST mediated miRNAs. Finally, lncRNA XIST maybe a useful biomarker regulating cisplatin resistance in lung cancer cells.Conclusions: LncRNA XIST competitively bound to miRNA 520 in the regulation of cisplatin resistance by BAX , participating apoptosis in the p53 signaling pathway.

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“…In Fig. 2 and Figure S2 a to d, we found that the expression levels of XIST, RELA, CD44, Slug, and ESA were remarkably decreased in the miR-7 mimic transiently transfected cells, especially in the case of XIST, which may regulate the stemness characteristics and tumorigenicity of some types of cancer cells, resulting in cancer progression [28][29][30][31][32][33]. To verify these claims, we attempted to identify whether XIST expression was regulated by miR-7/miR-92b.…”

Section: Discussionmentioning

confidence: 90%

MiR-7 reduces the BCSC subset by inhibiting XIST to modulate the miR-92b/Slug/ESA axis and inhibit tumor growth

Pan

You

et al. 2020

Breast Cancer Res

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Background: Breast cancer stem cells (BCSCs) are typically seed cells of breast tumor that initiate and maintain tumor growth. MiR-7, as a cancer inhibitor, decreases the BCSC subset and inhibits tumor progression through mechanisms that remain unknown. Methods: We examined miR-7 expression in breast cancer and developed a BCSC-driven xenograft mouse model, to evaluate the effects of miR-7 overexpression on the decrease of the BCSC subset in vitro and in vivo. In addition, we determined how miR-7 decreased the BCSC subset by using the ALDEFLUOR, lentivirus infection, dual-luciferase reporter, and chromatin immunoprecipitation-PCR assays. Results: MiR-7 was expressed at low levels in breast cancer tissues compared with normal tissues, and overexpression of miR-7 directly inhibited lncRNA XIST, which mediates the transcriptional silencing of genes on the X chromosome, and reduced epithelium-specific antigen (ESA) expression by increasing miR-92b and inhibiting slug. Moreover, miR-7 suppressed CD44 and ESA by directly inhibiting the NF-κB subunit RELA and slug in breast cancer cell lines and in BCSC-driven xenografts, which confirmed the antitumor activity in mice injected with miR-7 agomir or stably infected with lenti-miR-7. Conclusions: The findings from this study uncover the molecular mechanisms by which miR-7 inhibits XIST, modulates the miR-92b/Slug/ESA axis, and decreases the RELA and CD44 expression, resulting in a reduced BCSC subset and breast cancer growth inhibition. These findings suggest a potentially targeted treatment approach to breast cancer.

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Knockdown of LncRNA-XIST Suppresses Proliferation and TGF-β1-Induced EMT in NSCLC Through the Notch-1 Pathway by Regulation of miR-137

Abstract: We identified a branch of the XIST/miR-137/Notch-1 pathway that regulates proliferation and TGF-β1-induced EMT in NSCLC, which could be involved in NSCLC progression.

Cited by 67 publications

References 32 publications

LncRNA XIST acts as a microRNA-520 sponge to regulate the cisplatin resistance in NSCLC cells by mediating BAX through ceRNA network

LncRNA XIST acts as a microRNA-520 sponge to regulate the cisplatin resistance in NSCLC cells by mediating BAX through ceRNA network

LncRNA XIST acts as a microRNA-520 sponge to regulate the cisplatin resistance in NSCLC cells by mediating BAX through ceRNA network

MiR-7 reduces the BCSC subset by inhibiting XIST to modulate the miR-92b/Slug/ESA axis and inhibit tumor growth

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