Mitochondrial Metabolic Reprogramming and Nuclear Crosstalk in Cancer

Dear Colleagues,

Though aerobic glycolysis is an established phenomenon in cancer cells, recent developments in cancer metabolism suggest that most tumor mitochondria are not completely dysfunctional, but reprogram to have their ability to carry out oxidative phosphorylation (OXPHOS). Recently, increasing experimental evidence shows a critical role of OXPHOS in tumorigenesis and metastasis. Aggressively metastatic cancer cells, including tumor initiating cancer stem cells can acquire a stable ‘hybrid metabolic phenotype’ with high glycolytic and OXPHOS activity. Hybrid phenotype allows cancer cells to utilize multiple fuels for energy and to maintain a moderate reactive oxygen species (ROS) signalling. Extensive crosstalk between the mitochondria and the nucleus known as mitochondrial retrograde regulation (MRR), also influences many tumor and cellular activities. Importantly, several proto-oncogenes and tumor suppressors are actively involved in the regulation of metabolism. Many of them are known to locate inside the mitochondria but with unknown functional significance. Contrarily, metabolic reprogramming is also known to regulate the activation of oncoproteins by transcriptional and post-translational regulations. Recently, metabolically targeting of cancer cells is gaining increasing attention in oncology. Interestingly, repurposing of established metabolic targets like metformin is now considering for cancer prevention or therapy. Several metabolic targets are also now evaluating for sensitizing cancer cells to radiation and chemotherapy. Considering the heterogeneity of tumors, characterizing mitochondrial reprogramming and MRR in cancer subtypes is critical in understanding the mechanism of tumour initiation, progression and therapeutic resistance. It can also support the development of newer agents to metabolically target cancer subtypes and the repurposing of existing metabolic drugs for cancer therapy.

Dr. Benny Abraham Kaipparettu
Guest Editor

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