Unraveling the oncogenic role of LINC00504 and its interaction with miR-545-3p and ARIHI in hepatocellular carcinoma: novel insights for molecular therapy.

Objectives: Hepatocellular carcinoma (HCC) is a serious global health threat associated with high morbidity and mortality. The importance of long non-coding RNAs (lncRNAs) in tumor progression is growing. The aim of this study was to explore the expression, functional properties and molecular mechanisms of LINC00504 in HCC.

Materials And Methods: Tumor tissue samples from HCC patients were collected to analyze the expression of LINC00504, miR-545-3p, and ARIH1 mRNA using RT-qPCR, and compared with various HCC cell lines (PLC/PRF/5, SNU-182, Hep3B, HuH-7) and a human normal liver epithelial cell line (THLE-2). Cell proliferation, apoptosis, and invasion were assessed using transfection vectors, CCK8 assay, flow cytometry, and Transwell. Interactions among LINC00504, miR-545-3p, and ARIH1 were confirmed through database predictions and luciferase reporter gene assays.

Results: LINC00504 was underexpressed in HCC tissues and cell lines. Upregulation of LINC00504 inhibited cell proliferation, induced apoptosis, increased Bax and Caspase-3, decreased Bcl-2 mRNA, and suppressed invasion. miR-545-3p was overexpressed in HCC cells and was negatively regulated by LINC00504. Overexpression of miR-545-3p counteracted the effects of LINC00504 upregulation. ARIH1 was underexpressed in HCC tissues and had a negative correlation with miR-545-3p. miR-545-3p negatively regulated ARIH1 expression, and ARIH1 overexpression overturned the promotional effects of miR-545-3p on HCC cells.

Conclusion: This study uncovers the significant tumor-suppressing role of LINC00504 in HCC, potentially through a mechanism involving the targeting of miR-545-3p, which in turn inhibits the ARIH1. These findings offer new potential targets for HCC molecular treatment.