Open Access

ARTICLE

MiR-145-5p Suppresses Hepatocellular Carcinoma Progression by Targeting ABHD17C

Linpei Wang^1,#, Xiaoqiu Ma^2,#, Youqi Chen¹, Jiahui Zhang¹, Jiawei Zhang¹, Wei Wang^1,*, Shaojian Chen^3,*

1 Department of Hepatobiliary and Pancreatic Surgery, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, 362000, China
2 Department of Health Medicine, The 910th Hospital of People’s Liberation Army, Quanzhou, 362000, China
3 Department of General Surgery, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, 362000, China

* Corresponding Authors: Wei Wang. Email: ; Shaojian Chen. Email:
# These authors contributed equally in the study

Oncologie 2022, 24(4), 897-912. https://doi.org/10.32604/oncologie.2022.025693

Received 26 July 2022; Accepted 05 October 2022; Issue published 31 December 2022

Abstract

Background: MicroRNA-145-5p (miR-145-5p) reportedly inhibits hepatocellular carcinoma (HCC) by targeting ARF6, SPATS2, CDCA3, KLF5, and NRAS, indicating that miR-145-5p plays an important role in the occurrence and development of HCC by regulating the expression of various genes. In this study, we aimed to explore novel downstream targets of miR-145-5p and elucidate the potential mechanism of miR-145-5p in HCC. Materials and Methods: A bioinformatics analysis was performed to determine the clinical significance of miR-145-5p and alpha/beta hydrolase domain-containing protein 17C (ABHD17C) in patients with HCC. The ability of Hep3B cells to proliferate, migrate, and invade was examined after overexpression of miR-145-5p and ABHD17C or knockdown of ABHD17C. Tumorigenesis of Hep3B cells overexpressing miR-145 was detected using in vivo experiments. Results: miR-145-5p was downregulated in HCC tissues, and this was associated with poor prognosis in patients with HCC. Based on the bioinformatics analysis, miR-145-5p was predicted to target ABHD17C, as demonstrated by a luciferase reporter assay. ABHD17C downregulation inhibited cell viability, migration, and invasion and arrested the cell cycle. Overexpression of miR-145-5p significantly reduced the expression of ABHD17C. Moreover, ABHD17C expression was elevated in HCC tissues, which was associated with an unfavorable prognosis. Re-expressing ABHD17C into HCC cells rescued the suppressed cell viability, migration, and invasion mediated by ectopic expression of miR-145-5p. Importantly, miR-145-5p suppressed tumor growth in mice and downregulated the levels of Ki67 and ABHD17C in tumor. Conclusion: miR-145-5p could attenuate HCC progression via suppressing ABHD17C.

---

Keywords

---