MicroRNA-188-5p inhibits hepatocellular carcinoma proliferation and migration by targeting forkhead box N2

Autor: Yan-hui Wu, Bin Yu, Jiang-min Zhou, Xue-han Shen, Wei-xun Chen, Xi Ai, Chao Leng, Bin-yong Liang, Ya-jie Shao
Jazyk: angličtina
Rok vydání: 2023
Předmět:
Zdroj: BMC Cancer, Vol 23, Iss 1, Pp 1-13 (2023)
Druh dokumentu: article
ISSN: 1471-2407
DOI: 10.1186/s12885-023-10901-7
Popis: Abstract Background This study aimed to identify the biological functions, expression modes, and possible mechanisms underlying the relationship between metastatic human hepatocellular carcinoma (HCC) and MicroRNA-188-5p (miR-188) dysregulation using cell lines. Methods A decrease in miR-188 was detected in low and high metastatic HCC cells compared to that in normal hepatic cells and non-invasive cell lines. Gain- and loss-of-function experiments were performed in vitro to investigate the role of miR-188 in cancer cell (Hep3B, HepG2, HLF, and LM3) proliferation and migration. Results miR-188 mimic transfection inhibited the proliferation of metastatic HLF and LM3 cells but not non-invasive HepG2 and Hep3B cells; nonetheless, miR-188 suppression promoted the growth of HLF and LM3 cells. miR-188 upregulation inhibited the migratory rate and invasive capacity of HLF and LM3, rather than HepG2 and Hep3B cells, whereas transfection of a miR-188 inhibitor in HLF and LM3 cells had the opposite effects. Dual-luciferase reporter assays and bioinformatics prediction confirmed that miR-188 could directly target forkhead box N2 (FOXN2) in HLF and LM3 cells. Transfection of miR-188 mimics reduced FOXN2 levels, whereas miR-188 inhibition resulted in the opposite result, in HLF and LM3 cells. Overexpression of FOXN2 in HLF and LM3 cells abrogated miR-188 mimic-induced downregulation of proliferation, migration, and invasion. In addition, we found that miR-188 upregulation impaired tumor growth in vivo. Conclusions In summary, this study showed thatmiR-188 inhibits the proliferation and migration of metastatic HCC cells by targeting FOXN2.
Databáze: Directory of Open Access Journals
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