Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comment
. 2014 Feb;4(2):149-51.
doi: 10.1158/2159-8290.CD-13-1030.

EMT twists the road to PI3K

Matthew J Niederst  1 , Cyril H Benes
Affiliations
Comment

EMT twists the road to PI3K

Matthew J Niederst et al. Cancer Discov. 2014 Feb.

Abstract

Epithelial-to-mesenchymal transition (EMT) is important for many developmental events and has been linked to tumor dissemination and therapeutic resistance. Salt and colleagues identify how EMT affects how proliferation signals flow to phosphoinositide 3-kinase in non-small cell lung cancer.

PubMed Disclaimer

Figures

Figure 1
Figure 1
EMT status dictates treatment strategy in KRAS mutant NSCLCs. In epithelial cancers, the PI3K pathway can be blocked by inhibiting ErbB2 or ErbB3, while in mesenchymal cells, downregulation of ErbB3 and upregulation of other RTKs and PI3K suggest that these kinases should be targeted following an EMT.
See this image and copyright information in PMC

Comment on

References

    1. Polyak K, Weinberg RA. Transitions between epithelial and mesenchymal states: acquisition of malignant and stem cell traits. Nat Rev Cancer. 2009;9:265–73. - PubMed
    1. Singh A, Settleman J. EMT, cancer stem cells and drug resistance: an emerging axis of evil in the war on cancer. Oncogene. 2010;29:4741–51. - PMC - PubMed
    1. Salt MB, Bandyopadhyay S, McCormick F. Epithelial to mesenchymal transition rewires the molecular path to PI3-Kinase-dependent proliferation. Cancer Discov. 2013 - PubMed
    1. Wilson TR, Fridlyand J, Yan Y, Penuel E, Burton L, Chan E, et al. Widespread potential for growth-factor-driven resistance to anticancer kinase inhibitors. Nature. 2012;487:505–9. - PMC - PubMed
    1. Straussman R, Morikawa T, Shee K, Barzily-Rokni M, Qian ZR, Du J, et al. Tumour micro-environment elicits innate resistance to RAF inhibitors through HGF secretion. Nature. 2012;487:500–4. - PMC - PubMed

MeSH terms

Substances

LinkOut - more resources