Mitochondria and Cancer

By Sejal Vyas, Elma Zaganjor, M. Haigis. Cell, 2016

2,508 citations recorded by the source corpus.

Mitochondria are bioenergetic, biosynthetic and signaling organelles that are integral in stress sensing to allow for cellular adaptation to the environment. Therefore, it is not surprising that mitochondria are important mediators of tumorigenesis, as this process requires flexibility to adapt to cellular and environmental alterations in addition to cancer treatments. Multiple aspects of mitochondrial biology beyond bioenergetics support transformation including mitochondrial biogenesis and turnover, fission and fusion dynamics, cell death susceptibility, oxidative stress regulation, metabolism, and signaling. Thus, understanding mechanisms of mitochondrial misregulation during tumorigenesis will be critical for the next generation of cancer therapeutics.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/e8d39e6936a6b769b32a77c07758ea1eb9e74405

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Citations in the corpus

Lactate in the Regulation of Tumor Microenvironment and Therapeutic Approaches (2019, background): “Although defects in mitochondria function have been shown in some types of cancer (5), this process alone cannot explain the metabolic preference of tumor cells.”
Revisiting the hallmarks of cancer. (2017, positive): “While an initial explanation to the phenomenon was defective oxidative phosphorylation [148], it is now established that cancer cells (generally) have normally-functioning mitochondria capable of oxidative phosphorylation; in fact targeting mitochondrial DNA reduces tumorigenic potential of cells bo”
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Mitochondria and Cancer (2016, background): “NADPH for their own antioxidant defense (Figure 1) (Wallace, 2012).”
Mitochondrial metabolism and cancer (2017, background): “, malignant transformation, tumor progression and response to treatment, has eventually been given proper recognition [7, 8].”
Glutaminolysis: A Hallmark of Cancer Metabolism. (2017, background): “In addition to these pathways, mitochondrial ROS are mitigated by NADPH produced by an IDH1-driven reductive carboxylation reaction of glutamine in anchorage-independent growth conditions (91).”
Multi-omics analysis identifies ATF4 as a key regulator of the mitochondrial stress response in mammals (2017, background): “However, unlike in other diseases, here they are not at the origin of tumorigenesis; cancer cells modify cellular metabolism and mitochondrial function for their own purposes, using them as anabolic machines (Zong et al., 2016).”
Oxidative Phosphorylation as an Emerging Target in Cancer Therapy (2018, background): “It is also important tonote thatmanymtDNAmutations do not simply cause a decrease in OXPHOS but may facilitate adaptation to the bioenergetic demands of the tumor microenvironment without altering OXPHOS (6).”
The return of metabolism: biochemistry and physiology of the pentose phosphate pathway (2014, background): “…revealed that the patient carried an uncommon allelic combination: he is heterozygous for a catalytically inactive RPI allele, whereas the second allele encodes a partially catalytically functional enzyme that exhibits a cell-type-dependent expression deficit in addition (Wamelink et al., 2010).”
Supporting aspartate biosynthesis is an essential function of respiration in proliferating cells (2015, background): “Additionally, ETC activity impacts apoptosis (Newmeyer and FergusonMiller, 2003; Wallace, 2012), processes that depend on the mitochondrial membrane potential (Chen et al., 2014; Geissler et al., 2000), and reactive oxygen species (ROS) levels in cells (Schieber and Chandel, 2014).”
Recent insights into the function of autophagy in cancer (2016, background): “Given the recent appreciation for the importance of mitochondria in cancer (Zong et al. 2016), a selective form of autophagy of particular interest is that of mitophagy, which removes damaged mitochondria.”