Abstract
Introduction:
Hepatocellular carcinoma (HCC) accounts for 75–85% of primary liver cancer cases and remains a major cause of cancer-related mortality worldwide. Despite its high incidence, there is currently no definitive cure for most patients, and the underlying molecular mechanisms are not fully understood.
Methods:
HCC cells were used as an in vitro HCC model. Cells were divided into five groups: control, HnRNPA1 mimic, HnRNPA1 inhibitor, miR-23a-3p mimic, and miR-23a-3p inhibitor. HnRNPA1 and miR-23a-3p were overexpressed or silenced by transient transfection with specific mimics or inhibitors, respectively. Cell migration and apoptosis were assessed using Transwell assays and Annexin V/PI-based flow cytometry. The mRNA and protein expression levels of HnRNPA1, miR-23a-3p, PTEN, and related markers were measured by quantitative real-time PCR and Western blotting. Dual luciferase reporter assays were performed to validate the direct interaction between miR-23a-3p and the 3′ untranslated region of PTEN and to examine the regulatory relationship between HnRNPA1 and miR-23a-3p.
Results:
Overexpression of HnRNPA1 increased its mRNA level by approximately 2.5-fold compared with the control group (P
Discussion:
The research results show that HnRNPA1, miR-23a-3p, and PTEN play crucial roles in the progression of liver cancer. These molecules interact within a regulatory network that may become a therapeutic target.
Conclusion:
HnRNPA1, miR-23a-3p, and PTEN are key regulators of HCC progression and may serve as therapeutic targets for the treatment of HCC.