MiR‐101‐3p Regulates the Viability of Lung Squamous Carcinoma Cells via Targeting <i>EZH2</i>

Hou, Yu; Li, Lan; Ju, Yunhe; Lu, Yu‐Lin; Li, Chang; Xiang, Xudong

doi:10.1002/jcb.25836

Cited by 22 publications

(20 citation statements)

References 45 publications

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“…Importantly, better overall survival rates and disease-free survival time of NSCLC patients correlated with higher miR-101-3p expression levels. Thus, miR-101-3p could act as a useful indicator for NSCLC outcomes, which is in consistency with other reports [ 27 ].…”

Section: Discussionsupporting

confidence: 92%

Co-expression analysis revealed PTCH1-3'UTR promoted cell migration and invasion by activating miR-101-3p/SLC39A6 axis in non-small cell lung cancer: implicating the novel function of PTCH1

et al. 2017

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Metastasis is the most common cause of mortality for non-small cell lung cancer (NSCLC). PTCH1, a receptor of Hedgehog (Hh) pathway, is reported to suppress cell proliferation. Interestingly, our previous study showed PTCH1 silencing promoted cell proliferation but inhibited cell migration and invasion of NSCLC cells. However, the precise mechanisms of PTCH1 regulating NSCLC metastasis remain unclear. PTCH1 has multiple splicing variants, which all share the same 3’UTR sequence, meanwhile, emerging studies have shown competing endogenous RNAs (ceRNAs) play important roles in regulating cancer progression. Therefore, we hypothesized the functions of PTCH1-3’UTR in NSCLC in present study to reveal its role as a ceRNA. Here, we find overexpression of PTCH1-3’UTR promotes cell migration, invasion and adhesion, but does not affect cell proliferation in NSCLC cells. By combining weighted correlation network analysis (WGCNA) analysis and experimental validation, we reported PTCH1-3’UTR acted as a sponge to absorb miR-101-3p and promoted SLC39A6 expression. Moreover, we observed low expression of miR-101-3p and PTCH1 and high SLC39A6 levels were positively correlated with NSCLC progression. Therefore, our results help to understand the function of PTCH1 in NSCLC tumorigenesis and provide novel insights for the prevention of NSCLC metastasis.

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Section: Discussionsupporting

confidence: 92%

Co-expression analysis revealed PTCH1-3'UTR promoted cell migration and invasion by activating miR-101-3p/SLC39A6 axis in non-small cell lung cancer: implicating the novel function of PTCH1

et al. 2017

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“…In consideration of microRNAs paly their roles through regulating their target genes, such as miR-429 and BMI1 26, we predicted EZH2 gene might be a target of miR-101-3p by using online bioinformatics software. And, Hou Y reported miR-101-3p could regulate the proliferation of lung squamous carcinoma via targeting EZH2 27. EZH2 is an activator of gene expression, acting through multiple signaling pathways in distinct cancer types.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-101-3p advances cisplatin sensitivity in bladder urothelial carcinoma through targeted silencing EZH2

Li¹,

Xie²,

Zhang³

2019

J. Cancer

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Objective : Chemotherapy is a major therapeutic method for bladder urothelial carcinoma (BUC), which can effectively improve the prognosis of BUC patients, but the chemoresistance often leads to chemotherapy failure. This study will research the regulatory roles and molecular mechanism of miR-101-3p in BUC chemoresistance. Materials and Methods : The quantitative real-time PCR was used to detect the expression of miRNA-101-3p and EZH2. The proliferation and chemoresistance were analyzed by CCK8 assay. Luciferase reporter assay was used to verify the combination between miR-101-3p and EZH2. Protein expression was detected by Western blotting. Flow cytometry was used to examine apoptosis rate. Results : The miR-101-3p expression was down-regulated in cisplatin (CDDP) resistant BUC cell line (T24/CDDP) and tissues, and was positively related to sensitivity of BUC to CDDP. In T24/CDDP cells, the up-regulation of miR-101-3p decreased the half maximal inhibitory concentration (IC50) to CDDP, depressed the expression of MRP1 protein, promote the CDDP-induced cytotoxicity, and advanced CDDP sensitivity. A series of in vitro experiments certified the EZH2 gene was a target gene of miR-101-3p, including luciferase reporter assay, western blotting and so on. Up-regulation of EZH2 largely reversed the regulatory effects of miR-101-3p enhancement on CDDP sensitivity in T24/CDDP cells. Conclusion : The expression of miR-101-3p is positively related to CDDP sensitivity of BUC, miR-101-3p advances sensitivity of BUC to CDDP through targeted silencing EZH2.

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“…We further demonstrated direct binding between miR-101-3p and MALAT1 by dual luciferase reporter and RIP assays. MiR-101-3p is a tumor suppressor, which promotes apoptosis of endothelial cells and affects viability and invasiveness of squamous cell carcinoma [ 29 – 33 ]. In this study, we demonstrated high MALAT1 and low miR-101-3p levels in lung cancer A549 and H1299 cells.…”

Section: Discussionmentioning

confidence: 99%

MALAT1/miR-101-3p/MCL1 axis mediates cisplatin resistance in lung cancer

Wang

Zhang

et al. 2017

Oncotarget

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In this study, we investigated the mechanism by which lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) mediates cisplatin resistance in lung cancer. Lung cancer patients with high MALAT1 levels were associated with cisplatin resistance and low overall survival. Moreover, cisplatin-resistant A549/DDP cells showed higher MALAT1 expression than cisplatin-sensitive lung cancer cells (A549, H460, H1299 and SPC-A1). Dual luciferase reporter and RNA immunoprecipitation assays showed direct binding of miR-101-3p to MALAT1. MALAT1 knockdown in lung cancer cells resulted in miR-101-3p upregulation and increased cisplatin sensitivity. In addition, miR-101-3p decreased myeloid cell leukemia 1 (MCL1) expression by binding to the 3’-untranslated region (3’-UTR) of its mRNA. These results demonstrate that MALAT1/miR-101-3p/MCL1 signaling underlies cisplatin resistance in lung cancer.

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MiR‐101‐3p Regulates the Viability of Lung Squamous Carcinoma Cells via Targeting EZH2

Cited by 22 publications

References 45 publications

Co-expression analysis revealed PTCH1-3'UTR promoted cell migration and invasion by activating miR-101-3p/SLC39A6 axis in non-small cell lung cancer: implicating the novel function of PTCH1

Co-expression analysis revealed PTCH1-3'UTR promoted cell migration and invasion by activating miR-101-3p/SLC39A6 axis in non-small cell lung cancer: implicating the novel function of PTCH1

MicroRNA-101-3p advances cisplatin sensitivity in bladder urothelial carcinoma through targeted silencing EZH2

MALAT1/miR-101-3p/MCL1 axis mediates cisplatin resistance in lung cancer

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