Essentiality of fatty acid synthase in the 2D to anchorage-independent growth transition in transforming cells. Bueno, M. J., Jimenez-Renard, V., Samino, S., Capellades, J., Junza, A., López-Rodríguez, M. L., Garcia-Carceles, J., Lopez-Fabuel, I., Bolaños, J. P., Chandel, N. S., Yanes, O., Colomer, R., & Quintela-Fandino, M. Nature Communications, November, 2019. ![Essentiality of fatty acid synthase in the 2D to anchorage-independent growth transition in transforming cells [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex Upregulation of fatty acid synthase (FASN) is a common event in cancer, although its mechanistic and potential therapeutic roles are not completely understood. In this study, we establish a key role of FASN during transformation. FASN is required for eliciting the anaplerotic shift of the Krebs cycle observed in cancer cells. However, its main role is to consume acetyl-CoA, which unlocks isocitrate dehydrogenase (IDH)-dependent reductive carboxylation, producing the reductive power necessary to quench reactive oxygen species (ROS) originated during the switch from two-dimensional (2D) to three-dimensional (3D) growth (a necessary hallmark of cancer). Upregulation of FASN elicits the 2D-to-3D switch; however, FASN's synthetic product palmitate is dispensable for this process since cells satisfy their fatty acid requirements from the media. In vivo, genetic deletion or pharmacologic inhibition of FASN before oncogenic activation prevents tumor development and invasive growth. These results render FASN as a potential target for cancer prevention studies., The mechanisms associated with fatty acid synthase (FASN) upregulation during transformation are unclear. Here, the authors report that FASN promotes anaplerotic shift of the Krebs cycle in cancer cells expressing various oncogenes, and that its inhibition before transformation prevents tumour development and invasion.
@article{bueno_essentiality_2019,
title = {Essentiality of fatty acid synthase in the 2D to anchorage-independent growth transition in transforming cells},
volume = {10},
issn = {2041-1723},
url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6825217/},
doi = {10.1038/s41467-019-13028-1},
abstract = {Upregulation of fatty acid synthase (FASN) is a common event in cancer, although its mechanistic and potential therapeutic roles are not completely understood. In this study, we establish a key role of FASN during transformation. FASN is required for eliciting the anaplerotic shift of the Krebs cycle observed in cancer cells. However, its main role is to consume acetyl-CoA, which unlocks isocitrate dehydrogenase (IDH)-dependent reductive carboxylation, producing the reductive power necessary to quench reactive oxygen species (ROS) originated during the switch from two-dimensional (2D) to three-dimensional (3D) growth (a necessary hallmark of cancer). Upregulation of FASN elicits the 2D-to-3D switch; however, FASN's synthetic product palmitate is dispensable for this process since cells satisfy their fatty acid requirements from the media. In vivo, genetic deletion or pharmacologic inhibition of FASN before oncogenic activation prevents tumor development and invasive growth. These results render FASN as a potential target for cancer prevention studies., The mechanisms associated with fatty acid synthase (FASN) upregulation during transformation are unclear. Here, the authors report that FASN promotes anaplerotic shift of the Krebs cycle in cancer cells expressing various oncogenes, and that its inhibition before transformation prevents tumour development and invasion.},
urldate = {2019-11-15},
journal = {Nature Communications},
author = {Bueno, Maria J. and Jimenez-Renard, Veronica and Samino, Sara and Capellades, Jordi and Junza, Alejandra and López-Rodríguez, María Luz and Garcia-Carceles, Javier and Lopez-Fabuel, Irene and Bolaños, Juan P. and Chandel, Navdeep S. and Yanes, Oscar and Colomer, Ramon and Quintela-Fandino, Miguel},
month = nov,
year = {2019},
pmid = {31676791},
pmcid = {PMC6825217},
keywords = {Breast Cancer Clinical Research Unit, CNIO – Spanish National Cancer Research Center, Madrid, Spain, Breast cancer, CNIO, Cancer metabolism, Definiens Developer XD 2.5, Fluorescence quantification of membrane potential by TMRE in mitotracker-labelled mitochondria in cell cultures using Definiens Developer, IF quantification of FASN and 8-oxo-dG in double-stained tumor sections in murine model using Definiens Developer XD 2.5}
}
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