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The cylindromatosis gene (CYLD) encodes a deubiquitinase that was initiallyidentified as a tumor suppressor and has recently been investigated in connectionwith a variety of normal physiological processes. In contrast to its cell-proliferativeactivity, the effect of CYLD protein on cell migration has been a matter of debate.We investigated the effect of CYLD-siRNA on the migration activity of malignantmelanoma cells. Expression of CYLD mRNA/protein was lower in 6 of 8 malignantmelanoma cell lines than in 3 sets of primary-cultured normal human epidermalmelanocytes. Knockdown of CYLD significantly increased the proliferation activitiesof two melanoma cell lines (p&lt;0.05), along with BCL3 nuclear translocationfollowed by CCND1 overexpression. In contrast to the proliferation-related activity,CYLD knockdown significantly decreased the cell migration of all the melanomacell lines (n=7, p&lt;0.05), and we demonstrated that the mechanism regulatingmelanoma cell migration was activation of RAC1 through the action of CYLD. Ourfindings provide new insight into the role of CYLD-induced RAC1 activation inmelanoma cell migration.

international journal of oncology

Downregulation of cylindromatosis gene, CYLD, confers a growth advantage on malignant melanoma cells while negatively regulating their migration activity