Metabolic pathways promoting cancer cell survival and growth

Abstract

Activation of oncogenes and loss of tumour suppressors promote metabolic reprogramming in cancer, resulting in enhanced nutrient uptake to supply energetic and biosynthetic pathways. However, nutrient limitations within solid tumours may require that malignant cells exhibit metabolic flexibility to sustain growth and survival. Here, we highlight these adaptive mechanisms and also discuss emerging approaches to probe tumour metabolism in vivo and their potential to expand the metabolic repertoire of malignant cells even further.

Metabolic landscape of advanced gastric cancer according to HER2 and its prognostic implications

“…It also suggests that other factors besides HER2 influence hypermetabolism of gastric cancer. For example, tumor metabolism is consistently influenced by the mutation status of the MYC, TP53, and LKB1-AMPK-PI3 K pathway [28]. Therefore, cancer metabolism seems far more pleiotropic than it is expected to be.…”

Hepatocellular carcinoma redirects to ketolysis for progression under nutrition deprivation stress

“…Compared with their normal counterparts, cancer cells are metabolically reprogrammed in order to obtain sufficient energy or additional stimuli to support rapid cell growth and proliferation [1,2]. While cancer cells are known to consume glucose, glutamine and fatty acids disproportionately for energy as well as carbon and nitrogen sources for anabolism, nutrient limitation often occurs during tumor development.…”

Pharmacological inhibition of lipid droplet formation enhances the effectiveness of curcumin in glioblastoma

“…Although otherwise highly heterogeneous, most cancer types present a lipogenic phenotype characterized by the upregulation of key enzymes and transcriptional factors controlling lipid metabolism (e.g. Akt, fatty acid synthase, hypoxia-inducible factor 1-alpha, sterol regulatory element binding proteins, acetyl-CoA carboxylase alpha), and a boost in de novo lipogenesis [2][3][4][5]. In solid malignancies, the hypoxic conditions found at the core of the tumors induce adaptive pathways aimed at maintaining lipid synthesis, homeostatic pH and cell survival [6].…”