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Title 

Hypoxia-induced SM22α in A549 cells activates the IGF1R/PI3K/Akt pathway, conferring cellular resistance against chemo- and radiation therapy

Authors 

T R KimEun Wie ChoS G PaikI G Kim

Publisher 

Elsevier

Issue Date 

2012

Citation 

FEBS Letters, vol. 586, no. 4, pp. 303-309

Keywords 

Chemo-resistanceHypoxiaIGF1RβPI3K/AktSM22

Abstract 

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 Beta physically interacts with SM22 alpha by anti bait coimmunoprecipitation (View Interaction: 1, 2).

ISSN 

0014-5793

Link 

http://dx.doi.org/10.1016/j.febslet.2011.12.036

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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