Mitochondrial homeostasis and their impact on gastric carcinoma

Abstract

Gastric cancer is the fifth most diagnosed cancer and the third most common cause of cancer-related deaths worldwide. Mitochondrial dysfunction, with its impaired energy production and increased oxidative stress, fuels the development of gastric tumours. Gastric cancer exhibits dysregulated mitochondrial functions, which contribute to metabolic reprogramming, decreased apoptosis sensitivity, therapeutic resistance, and enhanced tumour progression and metastasis. In addition, aberrations in mitochondrial DNA, respiratory chain complexes, and epigenetic alterations foster a pro-tumorigenic microenvironment. Although significant progress has been made in understanding the various molecular mechanisms involved in gastric carcinogenesis, further studies are needed to elucidate mitochondrial homeostasis in gastric cancer. Unravelling mitochondrial intricacies in gastric cancer could open the development of definitive diagnostic and therapeutic interventions driving tumour growth. This review focuses on investigating the altered mitochondrial functionalities in gastric cancer.