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MicroRNA‐33b regulates hepatocellular carcinoma cell proliferation, apoptosis, and mobility via targeting Fli‐1‐mediated Notch1 pathway
Author(s) -
Wang Huiling,
Lin Xingtao,
Liu Entao,
Jian Zhixiang,
Ou Yingliang
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29673
Subject(s) - microrna , cancer research , cell growth , apoptosis , hepatocellular carcinoma , western blot , carcinogenesis , metastasis , cell , biology , effector , cell culture , microbiology and biotechnology , cancer , gene , genetics , biochemistry
MicroRNAs (miRNAs) have been confirmed to play pivotal roles in hepatocellular carcinoma (HCC) carcinogenesis. However, the underlying function of microRNA‐33b (miR‐33b) in HCC remains unclear. Here, we found that miR‐33b level was significantly reduced in both HCC tissues and tumor cell lines. Further, luciferase reporter assay and western blot analysis confirmed that Friend leukemia virus integration 1 (Fli‐1) was a direct target of miR‐33b. Overexpression of miR‐33b dramatically suppressed HCC tumor cell proliferation and cell mobility, but facilitated tumor cell apoptosis in vitro. Besides, restoration of Fli‐1 partially attenuated miR‐33b‐mediated inhibition of cell growth and metastasis via activating Notch1 signaling and its downstream effectors. Our findings demonstrate the important role of miR‐33b/Fli‐1 axis in HCC progression and provide novel therapeutic candidates for HCC clinical treatment.