ALKBH5 promotes Liver hepatocellular carcinoma cell proliferation, migration and invasion by regulating TTI1 expression

Abstract

Abstract Purpose The objective of this research was to investigate the potential mechanisms of ALKBH5 in Liver Hepatocellular Carcinoma (LIHC). Methods We examined the expression of ALKBH5 in pan-cancer and its correlation with clinical factors of LIHC. In vitro experiments were conducted to verify ALKBH5 expression in LIHC and its effect on LIHC cell proficiency. Differentially expressed genes (DEGs) were screened from LIHC patients associated with ALKBH5, and downstream genes associated with ALKBH5 were identified by bioinformatics analysis. We further examined the expression of the downstream genes and constructed a prognostic nomogram. Lastly, we analyzed the exact functions of ALKBH5 and TTI1 in LIHC cells. Results We found that ALKBH5 is significantly overexpressed in most pan-cancer types. In vitro experiments confirmed ALKBH5 as an oncogene in LIHC, with its knockdown suppressing the proliferation, migration, and invasion of LIHC cells. Bioinformatics analyses revealed that TTI1 is significantly positively correlated with ALKBH5. TTI1 was highly expressed in LIHC cells and has good prognostic ability for LIHC patients. Further experimental evidence confirmed that the suppression of TTI1 impeded cell proliferation, migration, and invasion, an impact partially offset by the overexpression of ALKBH5. In contrast, the promotion of these cellular progressions was observed with TTI1 overexpression but was tempered by a decrease in ALKBH5 expression. Conclusion In conclusion, our findings indicate that ALKBH5 may influence the proliferation, migration and invasion of LIHC by modulating TTI1 expression, providing a new direction for the treatment of LIHC.