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Endocrine-Related Cancer 15 (4) 965 -974     DOI: 10.1677/ERC-08-0030
Copyright © 2008 by the Society for Endocrinology
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The anandamide analog, Met-F-AEA, controls human breast cancer cell migration via the RHOA/RHO kinase signaling pathway

 Chiara Laezza1,2, Simona Pisanti 3, Anna Maria Malfitano3 and Maurizio Bifulco3

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.




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