Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Cells Tissues Organs. 2011;193(1-2):8-22. doi: 10.1159/000320172. Epub 2010 Nov 2.

Emergence of the phosphoinositide 3-kinase-Akt-mammalian target of rapamycin axis in transforming growth factor-β-induced epithelial-mesenchymal transition.

Author information

  • 1Department of Cell and Tissue Biology, Program in Cell Biology, University of California, San Francisco, CA 94143-0512, USA.

Abstract

During development and in pathological contexts such as fibrosis and cancer progression, epithelial cells can initiate a complex transcriptional reprogramming, accompanied by dramatic morphological changes, in a process named 'epithelial-mesenchymal transition' (EMT). In this transition, epithelial cells lose their epithelial characteristics to acquire mesenchymal properties and increased motile and invasive behavior. Transforming growth factor-β (TGF-β) has emerged as a major inducer of EMT through activation of downstream signaling pathways, including Smad and non-Smad signaling pathways. Among the non-Smad pathways, increasing evidence is emerging that the phosphoinositide 3-kinase-Akt-mammalian target of rapamycin axis plays a major role in TGF-β-induced EMT, notably through the regulation of translation and cell invasion. Pharmacological inhibitors of the phosphoinositide 3-kinase-Akt-mammalian target of rapamycin pathway may therefore represent an opportunity to selectively target essential aspects of TGF-β-induced EMT and provide an approach to prevent cancer cell dissemination toward metastasis, without the need to fully inactivate TGF-β signaling.

Copyright © 2010 S. Karger AG, Basel.

PMID:
21041997
[PubMed - indexed for MEDLINE]
PMCID:
PMC3030503
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for S. Karger AG, Basel, Switzerland Icon for PubMed Central
    Loading ...
    Write to the Help Desk