File:Model - TGF regulation of SHH.jpg: Difference between revisions

Schematic diagram showing activation of TGF-β receptor by TGF-β1which leads to the up-regulation of Shh expression

The secreted Shh protein then activates Hh signaling pathway by inhibition of Patched (smoothened suppressor), which will repress smoothened, resulting in the activation of GLI1 and its translocation to the nucleus. GLI1 as a Hh transcription factor then could activate Hh target genes, which leads to the acquisition of EMT phenotype, and contributing to increased invasion, metastasis and drug resistance.

"Our results show for the first time the transcriptional up-regulation of Shh by TGF-β1, which is mechanistically associated with TGF-β1 induced EMT phenotype and aggressive behavior of NSCLC cells. Thus the inhibitors of Shh signaling could be useful for the reversal of EMT phenotype, which would inhibit the metastatic potential of NSCLC cells and also make these tumors more sensitive to conventional therapeutics."

Original file name: Figure 9. Journal.pone.0016068.g009.png doi:10.1371/journal.pone.0016068.g009

Reference

PMC3020967 | PLoS ONE

Citation: Maitah MY, Ali S, Ahmad A, Gadgeel S, Sarkar FH (2011) Up-Regulation of Sonic Hedgehog Contributes to TGF-β1-Induced Epithelial to Mesenchymal Transition in NSCLC Cells. PLoS ONE 6(1): e16068. doi:10.1371/journal.pone.0016068

Editor: Irina Agoulnik, Florida International University, United States of America

Received: September 14, 2010; Accepted: December 5, 2010; Published: January 13, 2011

Copyright: © 2011 Maitah et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.