Alterations of mTOR signaling impact metabolic stress resistance in colorectal carcinomas with BRAF and KRAS mutations View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-12

AUTHORS

Raphaela Fritsche-Guenther, Christin Zasada, Guido Mastrobuoni, Nadine Royla, Roman Rainer, Florian Roßner, Matthias Pietzke, Edda Klipp, Christine Sers, Stefan Kempa

ABSTRACT

Metabolic reprogramming is as a hallmark of cancer, and several studies have reported that BRAF and KRAS tumors may be accompanied by a deregulation of cellular metabolism. We investigated how BRAFV600E and KRASG12V affect cell metabolism, stress resistance and signaling in colorectal carcinoma cells driven by these mutations. KRASG12V expressing cells are characterized by the induction of glycolysis, accumulation of lactic acid and sensitivity to glycolytic inhibition. Notably mathematical modelling confirmed the critical role of MCT1 designating the survival of KRASG12V cells. Carcinoma cells harboring BRAFV600E remain resistant towards alterations of glucose supply or application of signaling or metabolic inhibitors. Altogether these data demonstrate that an oncogene-specific decoupling of mTOR from AMPK or AKT signaling accounts for alterations of resistance mechanisms and metabolic phenotypes. Indeed the inhibition of mTOR in BRAFV600E cells counteracts the metabolic predisposition and demonstrates mTOR as a potential target in BRAFV600E-driven colorectal carcinomas. More... »

PAGES

9204

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41598-018-27394-1

    DOI

    http://dx.doi.org/10.1038/s41598-018-27394-1

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1104570305

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/29907857


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