mtDNA mutations increase tumorigenicity in prostate cancer.

By J. Petros, A. Baumann, E. Ruiz‐Pesini, M. Amin, C. Sun, John A. Hall, S. Lim, M. Issa, W. Flanders, S. Hosseini and 2 more. Proceedings of the National Academy of Sciences of the United States of America, 2005

862 citations recorded by the source corpus.

Subfields: Molecular Biology, Pulmonary and Respiratory Medicine, Spectroscopy

View Paper: https://www.semanticscholar.org/paper/0af8fd00aaf20fe2e13f78611b040621e5b4e6b1

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Citations in the corpus

Links between metabolism and cancer. (2012, background): “In this regard, experimental evidence through cybrid (fusing heterologous nuclei and cytoplasm from different cells) experiments supports a role for mtDNAmutations in enhanced tumorigenesis andmetastasis (Petros et al. 2005).”
Mitochondrial ATP synthase: architecture, function and pathology (2011, background): “8932C>T has, together with somatic mtDNA mutations in the cytochrome oxidase subunit I (COI) gene, been associated with prostate cancer (Petros et al. 2005; Arnold et al. 2009).”
Supporting aspartate biosynthesis is an essential function of respiration in proliferating cells (2015, background): “Mutations in ETC components resulting in partial inhibition of respiration may even be advantageous for proliferation in certain contexts by increasing ROS production (Petros et al., 2005).”
An enhanced MITOMAP with a global mtDNA mutational phylogeny (2006, background): “Since mtDNA mutations can arise in both the germline and somatic tissues, they have been associated with both degenerative diseases and cancers (4–6).”
HIF-1 inhibits mitochondrial biogenesis and cellular respiration in VHL-deficient renal cell carcinoma by repression of C-MYC activity. (2007, background): “Somatic mutations have been iden-tiﬁed in the mitochondrial genome of cancer cells (Polyak et al., 1998) and shown to promote tumor growth in xenograft assays (Petros et al., 2005).”
An essential role of the mitochondrial electron transport chain in cell proliferation is to enable aspartate synthesis (2015, background): “…effects, the mild ETC inhibition observed in cancer cells having heteroplasmic mtDNA mutations might have beneficial effects on tumorigenesis, likely not by affecting aspartate synthesis, but perhaps by increasing ROS levels (Ishikawa et al., 2008; Kulmacz, 1989; Petros et al., 2005).”
Prostate Cancer Review: Genetics, Diagnosis, Treatment Options, and Alternative Approaches (2022, background): “Mutations found in mitochondrial DNA genes have been found to cause prostate cancer [72].”
Oxidative Stress, Mitochondrial Dysfunction, and Aging (2011, background): “A better understanding of response to oxidative stress and mitochondrial dynamics will lead to new therapeutic approaches for the prevention or amelioration of age-associated degenerative diseases.”
Otto Warburg's contributions to current concepts of cancer metabolism (2011, background): “Do mtDNA mutations provide a survival and growth advantage to cancer cells? A compelling study by Wallace and co-worker”
Mitochondrial tumour suppressors: a genetic and biochemical update (2005, background): “Limited evidence does, however, indicate that some mitochondrial mutations might directly promote tumour growt”
Mitochondrial mutations in cancer (2006, background): “(Petros et al., 2005).”
Mitochondrial Energetics and Therapeutics (2010, positive): “Introduction of the pathogenic human mtDNA ATP6 8993T>G missense mutation into prostate cancer cells increased mitochondrial ROS production and prostate tumor growth (37), and the presence of the mtDNA ND6 13997G>A mutation increased the metastatic potential of mouse cancer cell lines in association”