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MicroRNA-301b promotes cell proliferation and apoptosis resistance in triple negative breast cancer by targeting CYLD
Hongming Song1, Dengfeng Li1, Tianqi Wu1, Dan Xie1, Kaiyao Hua1, Jiashu Hu1, Xiaochong Deng1, Changle Ji1, Yijun Deng1, Lin Fang1,*
1Department of Breast and Thyroid Surgery, Shanghai Tenth People’s Hospital, School of Medicine, Tongji University, 200072, Shanghai, China.
Aberrant expression of microRNAs (miRNAs) plays important roles in carcinogenesis and tumor progression. However, the expression and biological role of miR-301b in triple-negative breast cancer (TNBC) remains unclear. Here we aimed to evaluate the roles and mechanisms of miR-301b in TNBC cells. miR-301b expression was assessed in TNBC specimens and cell lines by quantitative Real-Time PCR (qRT-PCR). TNBC cells were transfected with miR-301b mimic or inhibitor or Cylindromatosis (CYLD) small interfering RNA (siRNA) using Lipofectamine 2000. The functional roles of miR-301b were determined by cell proliferation, colony formation, and apoptosis assays. Western blots and qRT-PCR were used to measure the expression of mRNAs and proteins in the cells. We found that miR-301b was upregulated in TNBC specimens and cell lines. Overexpression of miR-301b promoted cell proliferation in TNBC cells, while inhibited the apoptosis induced by 5-FU. CYLD was downregulated by miR-301b at both mRNA and protein levels in TNBC cells. Dual-luciferase report assay confirmed that miR-301b downregulated CYLD by direct interaction with the 3∏-untranslated region(3∏-UTR) of CYLD mRNA. NF-リB activation was mechanistically associated with miR-301b-mediated downregulation of CYLD. However, inhibition of miR-301b reversed all the effects of miR-301b. In conclusion, miR-301b plays an oncogenic role in TNBC possibly by downregulating CYLD and subsequently activating NF-リB p65, and this may provide a novel therapeutic approach for TNBC.
Abstract, Accepted Manuscript(in press) [Submitted on July 22, 2018, Accepted on September 27, 2018]
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