| Hypoxia-induced SM22α in A549 cells activates the IGF1R/PI3K/Akt pathway, conferring cellular resistance against chemo- and radiation therapy. | |
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MedLine Citation:
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PMID: 22245152 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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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). |
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Authors:
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Tae Rim Kim; Eun Wie Cho; Sang Gi Paik; In Gyu Kim |
Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-1-10 |
Journal Detail:
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Title: FEBS letters Volume: - ISSN: 1873-3468 ISO Abbreviation: - Publication Date: 2012 Jan |
Date Detail:
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Created Date: 2012-1-16 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0155157 Medline TA: FEBS Lett Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Copyright © 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved. |
Affiliation:
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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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