TI - The chromatin remodelling factor BRG1 is a novel binding partner of the tumor suppressor p16INK4a . AB - Background CDKN2A/p16INK4a is frequently altered in human cancers and it is the most important melanoma susceptibility gene identified to date . p16INK4a inhibits pRb PHOSphorylation and induces cell cycle arrest , which is considered its main tumour suppressor function . Nevertheless , additional activities may contribute to the tumour suppressor role of p16INK4a and could help explain its specific association with melanoma predisposition . To identify such functions we conducted a yeast-two hybrid screen for novel p16INK4a binding partners . Results We now report that p16INK4a interacts with the chromatin remodelling factor BRG1 . We investigated the cooperative roles of p16INK4a and BRG1 using a panel of cell lines and a melanoma cell model with inducible p16INK4a expression and BRG1 silencing . We found evidence that BRG1 is not required for p16INK4a -induced cell cycle inhibition and propose that the p16INK4a-BRG1 complex regulates BRG1 chromatin remodelling activity . Importantly , we found frequent loss of BRG1 expression in primary and metastatic melanomas , implicating this novel p16INK4a binding partner as an important tumour suppressor in melanoma . Conclusion This data adds to the increasing evidence implicating the SWI/SNF chromatin remodelling complex in tumour development and the association of p16INK4a with chromatin remodelling highlights potentially new functions that may be important in melanoma predisposition and chemoresistance .