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This Article Full Text Full Text (PDF) All Versions of this Article: ERC-08-0030v1 15/4/965    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Laezza, C. Articles by Bifulco, M. PubMed PubMed Citation Articles by Laezza, C. Articles by Bifulco, M.

¹ Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche, Napoli, Italy² Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università degli Studi di Napoli ‘Federico II,’ via Pansini, 80131 Napoli, Italy³ Dipartimento di Scienze Farmaceutiche, Università degli Studi di Salerno, Via Ponte don Melillo, 84084 Fisciano Salerno, Italy

(Correspondence should be addressed to C Laezza, IEOS, CNR, Via Pansini 5, 80131 Napoli, Italy; Email: chilaez{at}hotmail.com; M Bifulco; Email: maubiful{at}unina.it)

The endocannabinoid system regulates cell proliferation and migration in human breast cancer cells. In this study, we showed that a metabolically stable analog of anandamide, 2-methyl-2'-F-anandamide (Met-F-AEA), inhibited the RHOA activity and caused a RHOA delocalization from the cell membrane to cytosol determining a decrease in actin stress fibers. Overexpression of a dominant negative of RHOA activity and treatment of these cells with a RHO-associated protein kinase (ROCK) inhibitor, Y 27632, mimicked Met-F-AEA effects on actin organization and cell migration. We suggest that the inhibitory effect of Met-F-AEA on tumor cell migration could be related to RHOA-ROCK-dependent signaling pathway.