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Original Research Article | OPEN ACCESS

MiR-196b-5p regulates the proliferation of drug-resistant hepatocellular carcinoma cell lines by activating NF-κB/ABCB1 signaling pathway

Bangming Pu1, Yong Cao2, Yan Li2, Li Tang2, Jiyi Xia3, Bo Li1

1Department of Hepatobiliary Surgery; 2Medicine Experimental Center, The Affiliated Hospital of South West Medical University; 3School of Medical Information and Engineering, Southwest Medical University, Luzhou 646000, China.

For correspondence:-  Bo Li   Email: liboer2012@163.com   Tel:+868303160048

Accepted: 20 December 2019        Published: 31 January 2020

Citation: Pu B, Cao Y, Li Y, Tang L, Xia J, Li B. MiR-196b-5p regulates the proliferation of drug-resistant hepatocellular carcinoma cell lines by activating NF-κB/ABCB1 signaling pathway. Trop J Pharm Res 2020; 19(1):39-44 doi: 10.4314/tjpr.v19i1.6

© 2020 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To explore the molecular function of miR-196b-5p in hepatocellular carcinoma (HCC).
Methods: MiR-196b-5p expression levels in HCC tissue samples were assessed by qRT-PCR. MiR-196b-5p was knocked-down or over-expressed in HepG2 cells by transfecting the cells with plasmids expressing either a miR-196b-5p inhibitor or mimic, respectively, while cell proliferation was assessed by MTT assay. The interaction of miR-196b-5p with target molecules was confirmed using luciferase reporter assay. Cell cycle was investigated by flow cytometry, while NFκBIA expression was assessed by western blotting.
Results: MiR-196b-5p was over-expressed in HCC, and miR-196b-5p expression levels in patients with HCC were related to tumor grade. MiR-196b-5p over-expression promoted cell proliferation and colony formation and suppressed cell cycle arrest and apoptosis. The results of luciferase reporter assay showed that miR-196b-5p reduced NFκBIA expression in HepG2 cells by binding to a response element in the 3′ UTR of NFκBIA. Further investigation showed that NFκBIA interacts with NFκB1 and reduces the concentration of NFκB1 in HepG2 cells. The promoter of ATP-binding cassette sub-family B member 1 (ABCB1) was also targeted and bound by NFκB1, which altered the expression of ABCB1 in HepG2 cells.
Conclusion: MiR-196b-5p regulates cell proliferation in drug-resistant HCC cell lines via activation of the NFκB/ABCB1 signaling pathway.

Keywords: Hepatocellular carcinoma, miR-196b-5p, NF_4;BIA, NF_4;B1, ABCB1

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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