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Title: Increased expression of microRNA-31-5p inhibits cell proliferation, migration, and invasion via regulating Sp1 transcription factor in HepG2 hepatocellular carcinoma cell line

Abstract

Accumulating evidence has suggested that microRNA-31-5p (miR-31-5p) is dysfunctional in hepatocellular carcinoma (HCC). However, the molecular mechanism of HCC remains unclear. In this study, we investigated the role of miR-31-5p in tumor formation and development of HCC. The expression of miR-31-5p was detected in HCC tissues, corresponding adjacent tissues, normal liver tissues, and HCC cell lines. miR-31-5p mimics and an inhibitor were transfected into HepG2 cells to assess the effects of miR-31-5p on cell proliferation, apoptosis, cell cycle, migration, and invasion assays. Western blotting was used to detect the expression of Sp1 transcription factor (SP1), cyclin D1, and survivin in transfected HCC cells and control cells. The expression of miR-31-5p was significantly decreased in HCC cells and HCC tissues. Overexpression of miR-31-5p inhibited HCC cell growth, migration, and invasion. Overexpression of miR-31-5p reduced the expression of SP1 and cyclin D1, and knockdown of SP1 decreased cyclin D1 expression. The dual luciferase assay showed that miR-31-5p directly targeted SP1 in HepG2. Together, the results suggested that miR-31-5p acted as a tumor suppressor to regulate SP1, and that miR-31-5p could be used as a therapeutic target for the treatment of HCC. - Highlights: • The expression of miR-31-5p was significantly up-regulated inmore » HCC tissues. • Increased expression of miR-31-5p inhibits cell proliferation, migration, and invasion. • Sp1 transcription factor is the target gene for miR-31-5p.« less

Authors:
;  [1];  [2];  [3];  [1]
  1. Department of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Province (China)
  2. Department of Hepatobiliary Surgery, The First People's Hospital of Nanning, Nanning 530022, Guangxi Province (China)
  3. Department of Ultrasound, Shandong Provincial Hospital, Jinan 250021, Shandong Province (China)
Publication Date:
OSTI Identifier:
22719036
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 490; Journal Issue: 2; Other Information: Copyright (c) 2017 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ANIMAL TISSUES; APOPTOSIS; CELL CYCLE; CELL PROLIFERATION; HEPATOMAS; LIVER; LUCIFERASE; TRANSCRIPTION; TRANSCRIPTION FACTORS

Citation Formats

Zhao, Guoliang, Han, Chuangye, Zhang, Zhi, Wang, Lei, and Xu, Jing. Increased expression of microRNA-31-5p inhibits cell proliferation, migration, and invasion via regulating Sp1 transcription factor in HepG2 hepatocellular carcinoma cell line. United States: N. p., 2017. Web. doi:10.1016/J.BBRC.2017.06.050.
Zhao, Guoliang, Han, Chuangye, Zhang, Zhi, Wang, Lei, & Xu, Jing. Increased expression of microRNA-31-5p inhibits cell proliferation, migration, and invasion via regulating Sp1 transcription factor in HepG2 hepatocellular carcinoma cell line. United States. doi:10.1016/J.BBRC.2017.06.050.
Zhao, Guoliang, Han, Chuangye, Zhang, Zhi, Wang, Lei, and Xu, Jing. Sat . "Increased expression of microRNA-31-5p inhibits cell proliferation, migration, and invasion via regulating Sp1 transcription factor in HepG2 hepatocellular carcinoma cell line". United States. doi:10.1016/J.BBRC.2017.06.050.
@article{osti_22719036,
title = {Increased expression of microRNA-31-5p inhibits cell proliferation, migration, and invasion via regulating Sp1 transcription factor in HepG2 hepatocellular carcinoma cell line},
author = {Zhao, Guoliang and Han, Chuangye and Zhang, Zhi and Wang, Lei and Xu, Jing},
abstractNote = {Accumulating evidence has suggested that microRNA-31-5p (miR-31-5p) is dysfunctional in hepatocellular carcinoma (HCC). However, the molecular mechanism of HCC remains unclear. In this study, we investigated the role of miR-31-5p in tumor formation and development of HCC. The expression of miR-31-5p was detected in HCC tissues, corresponding adjacent tissues, normal liver tissues, and HCC cell lines. miR-31-5p mimics and an inhibitor were transfected into HepG2 cells to assess the effects of miR-31-5p on cell proliferation, apoptosis, cell cycle, migration, and invasion assays. Western blotting was used to detect the expression of Sp1 transcription factor (SP1), cyclin D1, and survivin in transfected HCC cells and control cells. The expression of miR-31-5p was significantly decreased in HCC cells and HCC tissues. Overexpression of miR-31-5p inhibited HCC cell growth, migration, and invasion. Overexpression of miR-31-5p reduced the expression of SP1 and cyclin D1, and knockdown of SP1 decreased cyclin D1 expression. The dual luciferase assay showed that miR-31-5p directly targeted SP1 in HepG2. Together, the results suggested that miR-31-5p acted as a tumor suppressor to regulate SP1, and that miR-31-5p could be used as a therapeutic target for the treatment of HCC. - Highlights: • The expression of miR-31-5p was significantly up-regulated in HCC tissues. • Increased expression of miR-31-5p inhibits cell proliferation, migration, and invasion. • Sp1 transcription factor is the target gene for miR-31-5p.},
doi = {10.1016/J.BBRC.2017.06.050},
journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 2,
volume = 490,
place = {United States},
year = {2017},
month = {8}
}