BMB Reports 2018; 51(11): 602-607  https://doi.org/10.5483/BMBRep.2018.51.11.168
MicroRNA-301b promotes cell proliferation and apoptosis resistance in triple-negative breast cancer by targeting CYLD
Hongming Song, Dengfeng Li, Tianqi Wu, Dan Xie, Kaiyao Hua, Jiashu Hu, Xiaochong Deng, Changle Ji, Yijun Deng & Lin Fang*
Department of Breast and Thyroid Surgery, Shanghai Tenth People’s Hospital, School of Medicine, Tongji University, Shanghai 200072, China
Correspondence to: Tel: +86-21-66307499; Fax: +86-21-66301869; E-mail: fanglin2017@126.com
Received: July 22, 2018; Revised: August 28, 2018; Accepted: September 27, 2018; Published online: November 30, 2018.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

cc This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
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 mimics, inhibitors 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-κB 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-κB p65, and this may provide a novel therapeutic approach for TNBC.
Keywords: Apoptosis, Cell proliferation, CYLD, MiR-301b, TNBC


This Article


Cited By Articles
  • CrossRef (0)

Funding Information

Collections

Services
Social Network Service

e-submission

Archives