Abstract
MiR-105 exerts inhibitory effects on the development and progression of various cancers, including breast cancer, lung cancer, and gastric cancer. Through GEO data analysis, we observed decreased expression of miR-105 in liver cancer tissues compared to adjacent tissues. Furthermore, miR-105 downregulates KIFC1 expression levels by targeting its 3' UTR. KIFC1 (Kinesin Family Member C1), a Protein Coding gene, may play a role in mitotic metaphase plate polymerization and mitotic spindle assembly. However, our findings suggest that this gene could serve as a potential chemotherapeutic target for Liver hepatocellular carcinoma (LIHC). We obtained the LIHC dataset from the TCGA database and genotype Tissue Expression Project (GTEx) normal tissue data for differential analysis. Additionally, we utilized the cBioPortal database, tumor immune single-cell center (TISCH) database, gene set enrichment analysis (GSEA), and R software to investigate the possible functions and mechanisms of KIFC1. These findings were further validated through experiments such as immunohistochemistry and wound healing assays. Our results indicate that KIFC1 might be involved in DNA repair and cell cycle regulation in LIHC cells which subsequently impacts tumor cell proliferation; moreover, miR-105 influences hepatoma cell line proliferation via its interaction with KIFC1. Collectively, these results highlight the potential therapeutic significance of targeting KIFC1 for chemotherapy treatment in LIHC patients.