PGC-1α mediates mitochondrial biogenesis and oxidative phosphorylation to promote metastasis

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PGC-1α mediates mitochondrial biogenesis and oxidative phosphorylation to promote metastasis

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Title: PGC-1α mediates mitochondrial biogenesis and oxidative phosphorylation to promote metastasis
Author: LeBleu, Valerie S.; O'Connell, Joyce T.; Herrera, Karina N. Gonzalez; Wikman-Kocher, Harriet; Pantel, Klaus; Haigis, Marcia C.; de Carvalho, Fernanda Machado; Damascena, Aline; Chinen, Ludmilla Thome Domingos; Rocha, Rafael M.; Asara, John M.; Kalluri, Raghu

Note: Order does not necessarily reflect citation order of authors.

Citation: LeBleu, V. S., J. T. O'Connell, K. N. G. Herrera, H. Wikman-Kocher, K. Pantel, M. C. Haigis, F. M. de Carvalho, et al. 2014. “PGC-1α mediates mitochondrial biogenesis and oxidative phosphorylation to promote metastasis.” Nature cell biology 16 (10): 992-15. doi:10.1038/ncb3039. http://dx.doi.org/10.1038/ncb3039.
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Abstract: Cancer cells can divert metabolites into anabolic pathways to support their rapid proliferation and to accumulate the cellular building blocks required for tumor growth. However, the specific bioenergetic profile of invasive and metastatic cancer cells is unknown. Here we report that migratory/invasive cancer cells specifically favor mitochondrial respiration and increased ATP production. Invasive cancer cells use transcription co-activator, PGC-1α to enhance oxidative phosphorylation, mitochondrial biogenesis and oxygen consumption rate. Clinical analysis of human invasive breast cancers revealed a strong correlation between PGC-1α expression in invasive cancer cells and formation of distant metastases. Silencing of PGC-1α in cancer cells suspended their invasive potential and attenuated metastasis without affecting proliferation, primary tumor growth or epithelial-to-mesenchymal (EMT) program. While inherent genetics of cancer cells determine the transcriptome framework required for invasion and metastasis, mitochondrial biogenesis and respiration induced by PGC-1α is also essential for functional motility of cancer cells and metastasis.
Published Version: doi:10.1038/ncb3039
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4369153/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:15034767
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