LIPID METABOLISM DISORDERS In PANCREATIC CANCER
I.N. Grigorieva1,2, O.V. Efimova1,3, T.I. Romanova1
1Institute of Internal and Preventive Medicine - Branch of Federal Reseach Institute of Cytology and Genetics of SB RAS, 630089, Novosibirsk, Boris Bogatkov str., 175/1
2Novosibirsk State National Research University, 630090, Novosibirsk, Pirogov str., 2
3City Clinical Hospital N 7, 630005, Novosibirsk, Olga Zhilina, 90а
Keywords: lipid metabolism, pancreatic cancer, gene TP53, KRAS, fatty acids
Abstract
In pancreatic cancer (PC) proved the role of obesity not only as a PC risk factor, but also as a factor associated with reduced survival in PC in adulthood. In PC is marked by increased lipogenesis: an increased need of cancer cells in the fatty acid (FA) is implemented not only by increasing lipogenesis de novo, but also by the exogenous FA assimilation, although several meta-analyses have not confirmed the importance of dietary fat in increasing the PC risk. Metabolic reprogramming of cancer cells is aimed at ensuring the rapid proliferation of tumor cells: the transition to aerobic glycolysis, increased expression of enzymes involved in the FA formation (citrate-synthase, ATP-citrate lyase and FA synthase - FASN), due to a mutation of the gene TP53 . As therapeutic agents in PC offer to inhibit FASN, and also impact prenylation and post-prenylation of oncogenes, in particular, KRAS , known as drugs, given the pleiotropic effect of atorvastatin and newly synthesized inhibitor farnesyltransferase R115777.
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