MDM2 promotes cell motility and invasiveness through a RING-finger independent mechanism

R Polanski, HE Warburton, A Ray-Sinha, T Devling, H Pakula, CARLOS RUBBI, N Vlatkovic, MT Boyd

Research output: Contribution to journalArticle (journal)peer-review

21 Citations (Scopus)


Recent studies connect MDM2 with increased cell motility, invasion and/or metastasis proposing an MDM2-mediated ubiquitylation-dependent mechanism. Interestingly, in renal cell carcinoma (RCC) p53/MDM2 co-expression is associated with reduced survival which is independently linked with metastasis. We therefore investigated whether expression of p53 and/or MDM2 promotes aggressive cell phenotypes. Our data demonstrate that MDM2 promotes increased motility and invasiveness in RCC cells (N.B. similar results are obtained in non-RCC cells). This study shows for the first time both that endogenous MDM2 significantly contributes to cell motility and that this does not depend upon the MDM2 RING-finger, i.e. is independent of ubiquitylation (and NEDDylation). Our data suggest that protein–protein interactions provide a likely mechanistic basis for MDM2-promoted motility which may constitute future therapeutic targets.
Original languageEnglish
Pages (from-to)4695-4702
JournalFEBS Letters
Publication statusPublished - 27 Oct 2010


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