| Literature DB >> 31564558 |
Pei-Hsuan Chen1, Ling Cai2, Kenneth Huffman3, Chendong Yang1, Jiyeon Kim1, Brandon Faubert1, Lindsey Boroughs1, Bookyung Ko1, Jessica Sudderth1, Elizabeth A McMillan4, Luc Girard5, Dong Chen6, Michael Peyton3, Misty D Shields3, Bo Yao7, David S Shames8, Hyun Seok Kim4, Brenda Timmons3, Ikuo Sekine3, Rebecca Britt3, Stephanie Weber3, Lauren A Byers9, John V Heymach9, Jing Chen6, Michael A White4, John D Minna10, Guanghua Xiao7, Ralph J DeBerardinis11.
Abstract
Intermediary metabolism in cancer cells is regulated by diverse cell-autonomous processes, including signal transduction and gene expression patterns, arising from specific oncogenotypes and cell lineages. Although it is well established that metabolic reprogramming is a hallmark of cancer, we lack a full view of the diversity of metabolic programs in cancer cells and an unbiased assessment of the associations between metabolic pathway preferences and other cell-autonomous processes. Here, we quantified metabolic features, mostly from the 13C enrichment of molecules from central carbon metabolism, in over 80 non-small cell lung cancer (NSCLC) cell lines cultured under identical conditions. Because these cell lines were extensively annotated for oncogenotype, gene expression, protein expression, and therapeutic sensitivity, the resulting database enables the user to uncover new relationships between metabolism and these orthogonal processes.Entities:
Keywords: (13)C stable isotope labeling; cancer metabolism; cell lines; gene expression; glucose; glutamine; non-small cell lung cancer; oncogenotypes; protein expression; therapeutic sensitivity
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Year: 2019 PMID： 31564558 PMCID： PMC6898782 DOI： 10.1016/j.molcel.2019.08.028
Source DB: PubMed Journal: Mol Cell ISSN： 1097-2765 Impact factor: 17.970