Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 407, Issue 1, Pages 181-184Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2011.02.134
Keywords
Fyn; IGF-beta1; E-cadherin; Snail; p38
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Funding
- Ministry for Health and Welfare, Republic of Korea [1020420]
- Korea Health Promotion Institute [1020420] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Transforming growth factor-beta (TGF-beta) signaling positively contributes to the regulation of tumor metastasis. However, the underlying molecular mechanisms are less well defined. We here show that Fyn, a member of Src family tyrosine kinases, plays a critical role in mediating TGF-beta 1-induced down-regulation of E-cadherin in human A549 lung cancer cells. Blockade of Fyn with siRNA knockdown or ligand-binding defective mutant significantly lowered the ability of TGF-beta 1 to repress E-cadherin expression. Furthermore, our results demonstrated that Fyn facilitates TGF-beta 1-mediated suppression of E-cadherin through p38 kinase-dependent induction of Snail. Collectively, our findings identify a Fyn-p38-Snail cascade as a new signaling pathway mediating oncogenic TGF-beta function. (C) 2011 Elsevier Inc. All rights reserved.
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