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MiR-33a functions as a tumor suppressor in triple-negative breast cancer by targeting EZH2

Authors
  • Weihua, Zeng1
  • Guorong, Zou1
  • Xiaolong, Cao1
  • Weizhan, Li1
  • 1 Guangzhou Panyu Central Hospital, No. 8, Fuyu East Road, Qiaonan Street, Panyu District, Guangzhou, 511486, People’s Republic of China , Guangzhou (China)
Type
Published Article
Journal
Cancer Cell International
Publisher
Springer (Biomed Central Ltd.)
Publication Date
Mar 18, 2020
Volume
20
Issue
1
Identifiers
DOI: 10.1186/s12935-020-1160-z
Source
Springer Nature
Keywords
License
Green

Abstract

BackgroundIncreasing reports have confirmed that microRNAs play an important role in breast cancer progression, particularly in triple-negative breast cancer (TNBC). The aim of our study was to investigate the role of miR-33a in TNBC progression.MethodsPCR assays were performed to detect miR-33a and EZH2 expression in TNBC tissues, adjacent nontumor tissues and cell lines. Western blot, CCK8, Transwell, cell colony formation and EdU cell proliferation, cell cycle analysis and luciferase reporter assays were used to determine the regulation of miR-33a/EZH2 in TNBC progression.ResultsMiR-33a was significantly downregulated in TNBC tissues and cell lines. MiR-33a overexpression in TNBC cells significantly inhibited cell growth and mobility and induced G1 cell cycle arrest. The luciferase reporter assay revealed that EZH2 is a direct target of miR-33a and that it was upregulated in TNBC tissues and cell lines. There was a negative correlation between miR-33a and EZH2 expression in TNBC tissues. EZH2 knockdown exerted similar inhibitory effects, while ectopic expression of EZH2 showed suppressive effects on malignant behaviors induced by miR-33a overexpression in TNBC cells.ConclusionsThese findings revealed that miR-33a is a tumor-suppressive miRNA in TNBC and can inhibit proliferation and mobility and induce G1 cell cycle arrest by directly targeting EZH2.

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