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

// Vera Dugina 1 , Natalya Khromova 2 , Vera Rybko 2 , Oleg Blizniukov 2 , Galina Shagieva 1 , Christine Chaponnier 3 , Boris Kopnin 2 and Pavel Kopnin 2 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.