AHCTF1 Functions as an Oncogenic Factor and Promotes Tumor Progression in Hepatocellular Carcinoma

Background Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality, with poor prognosis due to late diagnoses and limited therapeutic targets. The AT-hook containing transcription factor 1 (AHCTF1) is linked to various cancers, yet its role in HCC is unclear. Aims This study aimed to investigate AHCTF1's role in HCC progression. Methods Bioinformatics analysis was performed using The Cancer Genome Atlas (TCGA) database to evaluate AHCTF1 expression in HCC and normal tissues. Differentially expressed genes (DEGs) associated with AHCTF1 were identified and analyzed for enrichment in key signaling pathways. The function of AHCTF1 in HCC was assessed in vitro by overexpressing AHCTF1 in Huh7 cells and knocking it down in HepG2 cells. The effect of AHCTF1 on tumor growth and metastasis in vivo was validated through xenograft tumor models and lung metastasis models. Results AHCTF1 was significantly upregulated in HCC tissues and correlated with poor prognosis. Bioinformatics analysis demonstrated that DEGs associated with AHCTF1 were enriched in the PI3K-Akt and Hedgehog signaling pathways, cell adhesion, and glycolysis. Overexpression of AHCTF1 enhanced HCC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) process, while knockdown of AHCTF1 suppressed these malignant phenotypes. These findings have been validated through xenograft and lung metastasis models, and AHCTF1 promotes tumor growth and metastasis. Conclusion This study identifies AHCTF1 as a potential oncogenic factor, with high expression levels in HCC and a positive correlation with poor prognosis. AHCTF1 promotes tumor progression by enhancing the proliferation, migration, invasion, and EMT process of HCC cells.