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FAM83H-AS1/miR-485-5p/MEF2D axis facilitates proliferation, migration and invasion of hepatocellular carcinoma cells.

Authors :
Zhao, Wenpeng
Guo, Jiang
Li, Honglu
Cai, Liang
Duan, Youjia
Hou, Xiaopu
Diao, Zhenying
Shao, Xihong
Du, Hongliu
Li, Changqing
Source :
BMC Cancer. 12/7/2021, Vol. 21 Issue 1, p1-9. 9p.
Publication Year :
2021

Abstract

<bold>Background: </bold>Abundant evidence has manifested that long noncoding RNAs (lncRNAs) are closely implicated in human cancers, including hepatocellular carcinoma (HCC). Remarkably, lncRNA FAM83H antisense RNA 1 (FAM83H-AS1) has been reported to be a tumor-propeller in multiple cancers. However, its effect on HCC progression remains unknown.<bold>Methods: </bold>FAM83H-AS1 expression was analyzed by RT-qPCR. Colony formation, EdU, and flow cytometry as well as transwell assays were implemented to analyze the biological functions of FAM83H-AS1 on HCC progression. Luciferase reporter, RIP and RNA pull-down assays were implemented to detect the interaction among FAM83H-AS1, microRNA-485-5p (miR-485-5p), and myocyte enhancer factor 2D (MEF2D) in HCC cells.<bold>Results: </bold>FAM83H-AS1 expression in HCC cells was markedly elevated. FAM83H-AS1 accelerated cell proliferation, migration and invasion whereas inhibiting cell apoptosis in HCC. Besides, we confirmed that FAM83H-AS1 acts as a miR-485-5p sponge in HCC cells. Additionally, MEF2D was verified to be a direct target of miR-485-5p. FAM83H-AS1 could upregulate MEF2D expression via sponging miR-485-5p. Further, rescue experiments testified that MEF2D upregulation or miR-485-5p downregulation offset the repressive effect of FAM83H-AS1 depletion on HCC cell progression.<bold>Conclusions: </bold>FAM83H-AS1 facilitates HCC malignant progression via targeting miR-485-5p/MEF2D axis, suggesting that FAM83H-AS1 may be a promising biomarker for HCC treatment in the future. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
14712407
Volume :
21
Issue :
1
Database :
Academic Search Index
Journal :
BMC Cancer
Publication Type :
Academic Journal
Accession number :
153995651
Full Text :
https://doi.org/10.1186/s12885-021-08923-0