ArticleIn vitro cellular & developmental biology. Animal2026
Transcription factor HOXA4 promotes HBV replication and hepatocellular carcinoma proliferation by activating KIF11 transcription.
Article in In vitro cellular & developmental biology. Animal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
KIF11 is a mitotic kinesin responsible for the formation and maintenance of bipolar spindles, and it has high expression in the hepatocellular carcinoma (HCC). However, the role of the KIF11 gene in the hepatitis B virus (HBV)-related HCC remains unknown. Thus, this study aims to explore the function of transcription factor HOXA4 binding to KIF11 in HBV-related HCC, with the goal of providing a novel gene therapy approach for its treatment. HBV-positive (HepG2.2.15 cells) and HBV-negative (HepG2 cells) liver cancer cells were used to investigate the expression of KIF11 and HOXA4. HepG2 cells or HepG2.2.15 cells were transfected with the pc3.1-HBx, si-KIF11, and si-HOXA4, or co-transfected with the si-HOXA4 and oe-KIF11 for subsequent analysis. The binding of HOXA4 protein to the KIF11 gene promoter was examined based on a ChIP assay. The characteristics of HepG2.2.15 cells and HepG2 cells were assessed using CCK-8 and flow cytometry. HBV transcription and replication levels were detected via Northern and Southern blotting. The secretion level of HBV antigens in the HepG2.2.15 cell supernatant was measured by ELISA. KIF11 and HOXA4 were highly expressed in the HepG2.2.15 cells. Silencing KIF11 inhibited cell viability and HBV replication and transcription, reduced HBsAg and HBeAg levels in cell supernatants, promoted apoptosis, and downregulated p-PI3K/PI3K and p-AKT/AKT protein expression in HepG2.2.15 cells. pc3.1-HBx promoted cell viability, inhibited apoptosis, and upregulated p-PI3K/PI3K and p-AKT/AKT protein expression in HepG2 cells, which was reversed by si-KIF11. ChIP assays confirmed that HOXA4 bound to the KIF11 gene promoter. Silencing HOXA4 suppressed cell viability and HBV replication and transcription, decreased HBsAg and HBeAg levels in cell supernatants, enhanced apoptosis, and downregulated p-PI3K/PI3K and p-AKT/AKT protein expression in HepG2.2.15 cells. Silencing HOXA4 inhibited cell viability, promoted apoptosis, and downregulated p-PI3K/PI3K and p-AKT/AKT protein expression in HepG2 cells with pc3.1-HBx transfection. Overexpression of KIF11 counteracted the effects of si-HOXA4 in the HepG2.2.15 cells or HepG2 cells with pc3.1-HBx transfection. In conclusion, silencing of HOXA4 inhibited HBV replication and HCC proliferation by downregulating KIF11, providing a novel gene-assisted therapeutic approach for HBV-related HCC.
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