Doxorubicin (DOX) is a cornerstone chemotherapeutic drug in the treatment of hepatocellular carcinoma (HCC). However, its efficacy is often limited by the development of drug resistance linked to increased cellular capacity to repair DNA damage. Altered tumor metabolism allows cancer cells to meet increased energy demands for rapid proliferation while evading apoptosis and adapting to therapeutic interventions. MiR-203a-3p is associated with regulating members of the p53 family and has been impl
Regulation of doxorubicin resistance and cellular metabolism by miR-203a-3p via p53 and TAp63 signaling in hepatocellular carcinoma
Anwar Abdelnaser
