The tumor suppressor BAP1 cooperates with BRAFV600E to promote tumor formation in cutaneous melanoma

Pigment Cell & Melanoma Research
Joshua D WebsterAnwesha Dey

Abstract

The deubiquitinating enzyme BAP1 is mutated in a hereditary cancer syndrome with a high risk of mesothelioma and melanocytic tumors. Here, we show that Bap1 deletion in melanocytes cooperates with the constitutively active, oncogenic form of BRAF (BRAFV600E ) and UV to cause melanoma in mice, albeit at very low frequency. In addition, Bap1-null melanoma cells derived from mouse tumors are more aggressive and colonize and grow at distant sites more than their wild-type counterparts. Molecularly, Bap1-null melanoma cell lines have increased DNA damage measured by γH2aX and hyperubiquitination of histone H2a. Therapeutically, these Bap1-null tumors are completely responsive to BRAF- and MEK-targeted therapies. Therefore, BAP1 functions as a tumor suppressor and limits tumor progression in melanoma.

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Citations

Jul 22, 2020·Cancer Discovery·Michele CarboneGiovanni Gaudino
Jan 24, 2021·Cell Death Discovery·Aileen Patricia Szczepanski, Lu Wang
Jan 30, 2021·JCO Clinical Cancer Informatics·Sebastian WalpolePeter A Johansson
Apr 4, 2021·Journal of Clinical Medicine·Frédéric SoysouvanhRobert Ballotti
Dec 4, 2021·Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc·Michele DonatiDmitry V Kazakov

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