Document Detail

Hypoxia-induced SM22α in A549 cells activates the IGF1R/PI3K/Akt pathway, conferring cellular resistance against chemo- and radiation therapy.
MedLine Citation:
PMID:  22245152     Owner:  NLM     Status:  Publisher    
Chemo- or radiation-resistance in tumors caused by hypoxia often undermines efficacy of cancer therapy. Thus, therapies that overcome cellular resistance during hypoxia are necessary. SM22α is an actin-binding protein found in smooth muscle, fibroblasts, and some epithelium. We demonstrate that SM22α is induced in A549 non-small cell lung carcinoma cells by hypoxia and its overexpression increased chemo- and radiation-resistance. Hypoxia-mediated induction of SM22α expression is hypoxia-inducible factor-independent. Moreover, SM22α overexpression enhances tumor cell growth and activates the IGF1R/PI3K/Akt pathway via direct interaction with IGF1Rβ. Our results suggest SM22α as a novel regulator of hypoxic survival pathway of A549 NSCLC cells. STRUCTURED SUMMARY OF PROTEIN INTERACTIONS: IGFR1 Betaphysically interacts with SM22 alpha by anti bait coimmunoprecipitation (View Interaction: 1, 2).
Tae Rim Kim; Eun Wie Cho; Sang Gi Paik; In Gyu Kim
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-1-10
Journal Detail:
Title:  FEBS letters     Volume:  -     ISSN:  1873-3468     ISO Abbreviation:  -     Publication Date:  2012 Jan 
Date Detail:
Created Date:  2012-1-16     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0155157     Medline TA:  FEBS Lett     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
Department of Radiation Biology, Environmental Radiation Research Group, Korea Atomic Energy Research Institute, P.O. Box 105, Yuseong-gu, Daejeon 305-600, Republic of Korea.
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