Year: 2018
Type: article
Abstract: Since Otto Warburg first proposed that cancer cells have defective mitochondrial metabolism with enhanced aerobic glycolysis almost 100 years ago, uncovering the unique metabolic features of cancer has turned into one of the most vibrant and popular research areas in cancer research 1 . In contrast to Warburg’s idea of mitochondrial impairment, it is now evident that mitochondrial metabolism is largely intact, despite elevated glucose metabolism in cancer cells, and is even indispensable for tumor growth and survival 1 , 2 , 3 . Mitochondrial metabolic pathways, such as glutaminolysis, fatty acid oxidation, redox and one-carbon metabolism, are essential metabolic pathways for tumor growth and survival and thus are considered to be promising therapeutic targets for cancer therapy 4 . In addition, mitochondrial metabolism also confers resistance to conventional and targeted cancer therapy, implying that targeting mitochondrial metabolism could provide a promising combination strategy for cancer treatment 5 . Intriguingly, recent studies reveal that in addition to generating ATP, the mitochondrial electron transport chain is critical for tumor growth by providing an electron acceptor, such as NAD + , which is required for aspartate synthesis 6 , 7 . Importantly, it is now clear that the reprogramming of energy metabolism in cancer is directed by both intrinsic and extrinsic factors, such as oncogenic signaling and tumor microenvironment factors, which are actually known to cause cancer 8 , 9 .
Authors: Sang-Min Jeon, Nissim Hay
Institutions: Ajou University, University of Illinois Chicago
Language: English
Subfield: Cancer Research
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $4,490
Awards: G6846731920, G72484420, G8827280393
OpenAlex ID: W2808121706