Affiliations 

  • 1 Community Health Service Center, Zhongshan Street, Songjiang District, Shanghai, China
  • 2 Department of Hepatic Surgery, Kunshan Hospital of Traditional Chinese Medicine, Kunshan, Jiangsu Province, 215300, China
  • 3 The National University of Malaysia, Kuala Lumpur, Malaysia
  • 4 Department of Hepatic Surgery, Third Affiliated Hospital of Second Military Medical University, 225 Changhai Road, Shanghai, 200438, China. sunminmin_ehbh@126.com
  • 5 Community Health Service Center, Zhongshan Street, Songjiang District, Shanghai, China. lynnchan1001@163.com
Infect Agent Cancer, 2024 Dec 18;19(1):64.
PMID: 39696440 DOI: 10.1186/s13027-024-00628-w

Abstract

BACKGROUND/AIMS: microRNAs (miRNAs) contribute to tumorigenesis, progression and drug resistance of hepatocellular carcinoma (HCC). miR-3191 is a newly discovered miRNA, and its function and mechanism of action in biological processes and diseases are not completely understood.

METHODS: miR-3191 expression is determined via quantitative real-time polymerase chain reaction. Knockdown and overexpression of miR-3191 influence the proliferation and metastasis of HCC cells, which is measured by Cell Counting Kit-8 assay, Colony Formation assay and Cell metastasis assay. Protein expression is estimated by Western blot. The interplay between miR-3191 and target is validated by dual-luciferase reporter assay.

RESULTS: Here, we show that miR-3191 is upregulated in HCC tissues and associated with poor prognosis of HCC patients. Mechanistically, p21-activated protein kinase 6 (PAK6) was identified as a direct target of miR‑3191 in HCC. PAK6 knockdown partially recovered interference of miR‑3191‑induced decrease in cell proliferation and invasion. The accuracy of HCC patient prognosis could be improved by employing a combination of miR-3191 and PAK6 values.

CONCLUSIONS: miR-3191 promotes the proliferation and metastasis of HCC cells via targeting PAK6 and may serve as a prognostic biomarker and potential therapeutic target.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.