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MiRNA-107 enhances chemosensitivity to paclitaxel by targeting antiapoptotic factor Bcl-w in non small cell lung cancer.

ABSTRACT: The aim of this study is to elucidate whether and how miR-107 participates in the modulation of paclitaxel sensitivity in non small cell lung cancer (NSCLC). By qRT-PCR, we found that miR-107 is significantly down-regulated in paclitaxel-resistant A549/Taxol cells compared with corresponding paclitaxel-sensitive counterparts. Overexpression of miR-107 suppresses paclitaxel resistance of A549/Taxol cells through directly inhibiting Bcl-w. Overexpression of miR-107 promotes apoptosis and inhibits proliferation and mobility of A549/Taxol cells under treatment with paclitaxel in vitro. Moreover, miR-107 inhibits in vivo paclitaxel resistance in xenograft model. MiR-107/Bcl-w axis regulates paclitaxel chemoresistance through PI3K-Akt pathway. Our results suggest that up-regulation of miR-107 resensitizes paclitaxel-resistant NSCLC cells by targeting Bcl-w, which reveals a potential mechanism of miR-107 in reversing drug resistance.

SUBMITTER: Lu C

PROVIDER: S-EPMC5622221 | biostudies-other | 2017

REPOSITORIES: biostudies-other

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MiRNA-107 enhances chemosensitivity to paclitaxel by targeting antiapoptotic factor Bcl-w in non small cell lung cancer.

Lu Chaojing C Xie Zhibing Z Peng Qingzhen Q

American journal of cancer research 20170901 9

The aim of this study is to elucidate whether and how miR-107 participates in the modulation of paclitaxel sensitivity in non small cell lung cancer (NSCLC). By qRT-PCR, we found that miR-107 is significantly down-regulated in paclitaxel-resistant A549/Taxol cells compared with corresponding paclitaxel-sensitive counterparts. Overexpression of miR-107 suppresses paclitaxel resistance of A549/Taxol cells through directly inhibiting Bcl-w. Overexpression of miR-107 promotes apoptosis and inhibits ...[more]

PMID: 28979809

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Project description:UnlabelledHepatitis C virus (HCV)-mediated liver diseases are one of the major health issues in the United States and worldwide. HCV infection has been reported to modulate microRNAs (miRNAs) that control various cell surface receptors and gene-regulatory complexes involved in hepatic inflammation and liver diseases. We report here that specific downregulation of miRNA-107 and miRNA-449a following HCV infection in patients with HCV-mediated liver diseases modulates expression of CCL2, an inflammatory chemokine upregulated in patients with chronic liver diseases, by targeting components of the interleukin-6 receptor (IL-6R) complex. Computational analysis for DNA-bound transcription factors in the CCL2 promoter identified adjacent binding sites for CCAAT/CEBP?, spleen focus-forming virus, proviral integration oncogene (SPI1/PU.1), and STAT3. We demonstrate that CEBP?, PU.1, and STAT3 interacted with each other physically to cooperatively bind to the promoter and activate CCL2 expression. Analysis of IL-6R and JAK1 expression in HCV patients by quantitative PCR showed significant upregulation when there was impaired miRNA-107 and miRNA-449a expression, along with upregulation of PU.1 and STAT3, but not CEBP?. miRNA-449a and miRNA-107 target expression of IL-6R and JAK1, respectively, in vitro and also inhibit IL-6 signaling and impair STAT3 activation in human hepatocytes. Taken together, our results demonstrate a novel gene-regulatory mechanism in which HCV-induced changes in miRNAs (miRNA-449a and miRNA-107) regulate CCL2 expression by activation of the IL-6-mediated signaling cascade, which we propose will result in HCV-mediated induction of inflammatory responses and fibrosis.ImportanceHepatitis C virus (HCV)-induced hepatitis is a major health concern worldwide. HCV infection results in modulation of noncoding microRNAs affecting major cellular pathways, including inflammatory responses. In this study, we have identified a microRNA-regulated pathway for the chemokine CCL2 in HCV-induced hepatitis. Understanding microRNA-mediated transcriptional-regulatory pathways will result in development of noninvasive biomarkers for better disease prediction and development of effective therapeutics.

Dataset Information

MiRNA-107 enhances chemosensitivity to paclitaxel by targeting antiapoptotic factor Bcl-w in non small cell lung cancer.

Publications

MiRNA-107 enhances chemosensitivity to paclitaxel by targeting antiapoptotic factor Bcl-w in non small cell lung cancer.

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