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Gene mutations cause reprogramming of lipid metabolism in pancreatic cancer cells to meet their proliferation needs This is reflected in the increased de novo synthesis of fatty acids, enhanced activities of various rate-limiting enzymes, and upregulated expression of receptors for transporting exogenous cholesterol and lipid droplets. The synthesized lipids satisfy the proliferation and survival of pancreatic cancer and signal transduction.
Source publication
The pathogenesis of pancreatic cancer involves substantial metabolic reprogramming, resulting in abnormal proliferation of tumor cells. This tumorigenic reprogramming is often driven by genetic mutations, such as activating mutations of the KRAS oncogene and inactivating or deletions of the tumor suppressor genes SMAD4, CDKN2A, and TP53, which play...
Context in source publication
Context 1
... process includes the following main characteristics: the de novo synthesis of fatty acids is increased, while the oxidation of fatty acids is decreased to meet the needs of tumor cell proliferation. The upregulation of lipid metabolism-related proteins and enzymes promotes malignant tumor progression ( Figure 3) [80][81][82]. De novo fatty acid synthesis is first catalyzed by ATP citrate lyase (ACLY) to generate acetyl coenzyme A (acetyl-CoA); then, acetyl-CoA is carboxylated by acetyl-CoA carboxylase (ACC) to generate malonyl coenzyme A (malonyl-CoA). ...
