Oncotarget

Research Papers:

Tumor promotion by γ and suppression by β non-muscle actin isoforms

Vera Dugina, Natalya Khromova, Vera Rybko, Oleg Blizniukov, Galina Shagieva, Christine Chaponnier, Boris Kopnin and Pavel Kopnin _

PDF  |  HTML  |  Supplementary Files  |  How to cite

Oncotarget. 2015; 6:14556-14571. https://doi.org/10.18632/oncotarget.3989

Metrics: PDF 1610 views  |   HTML 2849 views  |   ?  


Abstract

Vera Dugina1, Natalya Khromova2, Vera Rybko2, Oleg Blizniukov2, Galina Shagieva1, Christine Chaponnier3, Boris Kopnin2 and Pavel Kopnin2

1 Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russia

2 Blokhin Russian Cancer Research Center, Moscow, Russia

3 Department of Pathology and Immunology, Faculty of Medicine, University of Geneva, CMU, Geneva, Switzerland

Correspondence to:

Pavel Kopnin, email:

Keywords: cancer, actin isoforms, ERK1/2, PP1, p34-Arc, WAVE, cofilin1

Received: March 06, 2015 Accepted: April 15, 2015 Published: May 04, 2015

Abstract

Here we have shown that β-cytoplasmic actin acts as a tumor suppressor, inhibiting cell growth and invasion in vitro and tumor growth in vivo. In contrast, γ-cytoplasmic actin increases the oncogenic potential via ERK1/2, p34-Arc, WAVE2, cofilin1, PP1 and other regulatory proteins. There is a positive feedback loop between γ-actin expression and ERK1/2 activation. We conclude that non-muscle actin isoforms should not be considered as merely housekeeping proteins and the β/γ-actins ratio can be used as an oncogenic marker at least for lung and colon carcinomas. Agents that increase β- and/or decrease γ-actin expression may be useful for anticancer therapy.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 3989