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