Literature DB >> 24576621

Combination PI3K/MEK inhibition promotes tumor apoptosis and regression in PIK3CA wild-type, KRAS mutant colorectal cancer.

Jatin Roper1, Mark J Sinnamon2, Erin M Coffee3, Peter Belmont4, Lily Keung5, Larissa Georgeon-Richard6, Wei Vivian Wang6, Anthony C Faber3, Jihye Yun7, Ömer H Yilmaz8, Roderick T Bronson9, Eric S Martin9, Philip N Tsichlis5, Kenneth E Hung10.   

Abstract

PI3K inhibition in combination with other agents has not been studied in the context of PIK3CA wild-type, KRAS mutant cancer. In a screen of phospho-kinases, PI3K inhibition of KRAS mutant colorectal cancer cells activated the MAPK pathway. Combination PI3K/MEK inhibition with NVP-BKM120 and PD-0325901 induced tumor regression in a mouse model of PIK3CA wild-type, KRAS mutant colorectal cancer, which was mediated by inhibition of mTORC1, inhibition of MCL-1, and activation of BIM. These findings implicate mitochondrial-dependent apoptotic mechanisms as determinants for the efficacy of PI3K/MEK inhibition in the treatment of PIK3CA wild-type, KRAS mutant cancer.
Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

Entities:  

Keywords:  Colorectal cancer; KRAS; MEK; Mouse model of cancer; PI3K

Mesh：

Substances：

Year:  2014        PMID： 24576621      PMCID： PMC4118771          DOI： 10.1016/j.canlet.2014.02.018

Source DB:  PubMed          Journal:  Cancer Lett        ISSN： 0304-3835            Impact factor:   8.679


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