Metabolic Reprogramming in Cancer
A special issue of Cells (ISSN 2073-4409).
Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 961
Special Issue Editor
Interests: cancer; mitochondrial metabolism; metabolic reprogramming; hybrid metabolic status; transmitochondrial cybrids and fatty acid oxidation
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Recent developments in cancer metabolism suggest that most tumor mitochondria are not dysfunctional, but are reprogrammed to have their ability to carry out oxidative phosphorylation (OXPHOS). Metabolic reprogramming is an effective way for cancer cells to reorganize their metabolic pathways and to effectively use all of the available resources for its high energy demand. As mitochondria have energy sources other than glucose, like fatty acid and glutamine, metabolic reprogramming will allow cancer cells to utilize such alternative pathways as an energy source. Aggressively metastatic cancer cells and tumour initiating cancer stem cells can acquire a stable “hybrid metabolic phenotype” with a high glycolytic and OXPHOS activity. A hybrid phenotype allows cancer cells to utilize multiple fuels for energy and to maintain moderate reactive oxygen species (ROS) signalling. Extensive crosstalk between the mitochondria and the nucleus also influences many tumour and cellular activities. Importantly, several proto-oncogenes and tumor suppressors are actively involved in the regulation of metabolism. Many such nuclear DNA encoded proteins are known to be located inside the mitochondria, but with unknown functional significance. Contrarily, mitochondrial metabolism is also known to regulate the activation of oncoproteins through transcriptional and post-translational regulations. Recently, the metabolically targeting of cancer cells has been receiving increased attention in oncology. The repurposing of established metabolic targets, like the metformin, is now being considered for cancer prevention or therapy. Understanding more mechanisms of mitochondrial reprogramming in cancer can support the development of newer agents to metabolically target cancer subtypes and to repurpose the existing metabolic drugs for cancer therapy.
Dr. Benny Abraham Kaipparettu
Guest Editor
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