Deciphering the Role of Mitochondrial DNA Targeted Therapy in Hepatic Cell Carcinoma

Liver cancer, also identified as hepatic cell carcinoma, is the fifth most prevalent kind of malignancy globally and the fourth foremost cause of cancer-associated mortality. The development and progression of liver cancer are complex processes that involve multiple genetic and environmental factors. As the diagnosis of liver cancer is still worse, with late-stage patients facing a less than 20% 5-year survival rate, there is a critical need for the development of new and effective therapeutic approaches for liver cancer. Mitochondrial alterations and mitochondrial DNA (mtDNA) mutations have long been associated with cancer pathogenesis, including liver cancer. These alterations not only disrupt cellular bioenergetics but also deteriorate the situation by modifying tumor suppressors and oncogenic proteins. Excessive reactive oxygen species generation and flaws in mitochondrial enzymes are among the factors responsible for mitochondrial dysfunction. Additionally, perturbed microRNA levels have also been linked to mtDNA dysfunction and reactive oxygen species generation. Various pharmacological approaches to target mitochondrial dysfunction and mtDNA mutations in cancer have been proposed as potential therapeutic strategies. These approaches include targeting the electron transport chain, which is responsible for the production of adenosine triphosphate in the mitochondria, or transcriptional inhibition of various proteins involved in the mitochondrial biogenesis pathway. Overall, mtDNA is a crucial component of the cell, and alterations in mtDNA make it an attractive target for therapeutic interventions. Hence, we advocate that understanding the role of mtDNA in cancer pathogenesis is important for the development of targeted therapies for these disorders.