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

36Citations
Citations of this article
16Readers
Mendeley users who have this article in their library.

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). © 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

Cite

CITATION STYLE

APA

Kim, T. R., Cho, E. W., Paik, S. G., & Kim, I. G. (2012). Hypoxia-induced SM22α in A549 cells activates the IGF1R/PI3K/Akt pathway, conferring cellular resistance against chemo- and radiation therapy. FEBS Letters, 586(4), 303–309. https://doi.org/10.1016/j.febslet.2011.12.036

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free