Metabolic pathways promoting cancer cell survival and growth

By Lindsey K. Boroughs, Ralph J. Deberardinis. Nature Cell Biology, 2015

1,329 citations recorded by the source corpus.

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.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/928c91cdc48e0dbb8781394c6f9f0ddc23c017da

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Citations in the corpus

Fundamentals of cancer metabolism (2016, background): “Themetabolic flexibility afforded by multiple inputs into the TCA cycle allows cancer cells to adequately respond to the fuels available in the changing microenvironment during the evolution of the tumor (9).”
Metabolic heterogeneity in human lung tumors (2016, positive): “Although glucose is a prominent energy source, emerging evidence indicates that tumor cells oxidize other nutrients as well, and in some circumstances may prefer alternative fuels to glucose (Boroughs and DeBerardinis, 2015; Mashimo et al., 2014).”
Reprogramming of glucose, fatty acid and amino acid metabolism for cancer progression (2015, background): “GLUT1, glucose transporter 1, was transactivated by oncogenes cMyc, KRas and HIF-1a, but inhibited by tumor suppressor p53 [31].”
CD8+ T cells and fatty acids orchestrate tumor ferroptosis and immunity via ACSL4 (2022, background): “Along this line, metabolic reprogramming occurs in tumorigenesis (Boroughs and DeBerardinis, 2015) and cancer immunotherapy (Li et al., 2019).”
Acetyl coenzyme A: a central metabolite and second messenger. (2015, background): “Metabolic Fate of Mitochondrial Acetyl-CoA Normally, mitochondrial acetyl-CoA is metabolized within the TCA to yield NADH, the main substrate for ATP synthesis via oxidative phosphorylation (Boroughs and DeBerardinis, 2015).”
Amino acid transporter SLC7A11/xCT at the crossroads of regulating redox homeostasis and nutrient dependency of cancer (2018, background): “Specifically, glucose and glutamine supplies are often limited in tumor cells within a tumor mass because of poor tumor vasculature in the tumor microenvironment [68].”