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

Here we have shown that beta-cytoplasmic actin acts as a tumor suppressor, inhibiting cell growth and invasion in vitro and tumor growth in vivo. In contrast, gamma-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 gamma-actin expression and ERK1/ 2 activation. We conclude that non-muscle actin isoforms should not be considered as merely housekeeping proteins and the beta/gamma-actins ratio can be used as an oncogenic marker at least for lung and colon carcinomas. Agents that increase beta- and/or decrease gamma-actin expression may be useful for anticancer therapy.