Mitochondria and cancer

By Douglas C. Wallace. Nature Reviews. Cancer, 2012

1,519 citations recorded by the source corpus.

Contrary to conventional wisdom, functional mitochondria are essential for the cancer cell. Although mutations in mitochondrial genes are common in cancer cells, they do not inactivate mitochondrial energy metabolism but rather alter the mitochondrial bioenergetic and biosynthetic state. These states communicate with the nucleus through mitochondrial 'retrograde signalling' to modulate signal transduction pathways, transcriptional circuits and chromatin structure to meet the perceived mitochondrial and nuclear requirements of the cancer cell. Cancer cells then reprogramme adjacent stromal cells to optimize the cancer cell environment. These alterations activate out-of-context programmes that are important in development, stress response, wound healing and nutritional status.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/c319c7cf2ee6a2981e7bbbafcc89ea3791beba6f

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Citations in the corpus

Mitochondrial dynamics in health and disease: mechanisms and potential targets (2023, background): “232 Moreover, numerous immune functions depend on the proper ef ﬁ ciency of mitochondrial metabolism in immunocytes.”
The return of metabolism: biochemistry and physiology of the pentose phosphate pathway (2014, neutral): “…(Alzheimer’s disease), cardiovascular disease, parasite infections and cancer (Wood, 1985; Zimmer, 1992; Zimmer, 2001; Schaaff-Gerstenschlager & Zimmermann, 1993; Gupte, 2008; Mayr et al., 2008; Orešič et al., 2011; Vander Heiden et al., 2011; Riganti et al., 2012; Wallace, 2012).”
Mitochondrial DNA genetics and the heteroplasmy conundrum in evolution and disease. (2013, background): “When mitochondria experience extreme stress (elevated Ca2þ and ROS, depleted adenine nucleotides, and reduced membrane potential), this can activate the mitochondrial permeability transition pore (mtPTP) thus initiating apoptosis and necrosis (Wallace 2005, 2011, 2012, 2013a,b; Wallace et al. 2013).”
MYC, metabolism, cell growth, and tumorigenesis. (2013, background): “In addition to respiration, mitochondria mediate many biosynthetic pathways (Wallace 2012).”
Acetyl coenzyme A: a central metabolite and second messenger. (2015, background): “…(mitochondrial carrier; dicarboxylate transporter), member 10 (SLC25A10), an inorganic phosphate/dicarboxylate antiporter (Mizuarai et al., 2005), or solute carrier family 25 (mitochondrial carrier; oxoglutarate carrier), member 11 (SLC25A11), an a-ketoglutarate/malate antiporter (Wallace, 2012).”