BAP1 regulates cell cycle progression through E2F1 target genes and mediates transcriptional silencing via H2A monoubiquitination in uveal melanoma cells

Pan, Hui; Jia, Renbing; Zhang, Leilei; Xu, Shi-Qiong; Wu, Qing; Song, Xin; Zhang, He; Ge, Shengfang; Xu, Xiaofei

doi:10.1016/j.biocel.2015.01.001

Cited by 51 publications

(40 citation statements)

References 37 publications

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“…In fact, its loss has been associated with the tumorigenesis of 92.1 uveal melanoma cells [19]. On the other hand, its knockdown down-regulated E2F1 target genes, resulting in the blockade of S phase initiation, cell growth and invasiveness in OCM1 and OM431 uveal melanoma cells [20]. Depletion of BAP1 expression in cutaneous melanoma cells reduced proliferation and induced apoptosis, inhibiting tumor growth in vivo, but its overexpression in melanocytes suppressed proliferation [21].…”

Section: Bap1mentioning

confidence: 98%

BAP1,PBRM1andSETD2in clear-cell renal cell carcinoma: molecular diagnostics and possible targets for personalized therapies

Piva¹,

Santoni

Matrana

et al. 2015

Expert Review of Molecular Diagnostics

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Several novel recurrent mutations of histone modifying and chromatin remodeling genes have been identified in renal cell carcinoma. These mutations cause loss of function of several genes located in close proximity to VHL and include PBRM1, BAP1 and SETD2. PBRM1 encodes for BAF180, a component of the SWI/SNF chromatin remodeling complex, and is inactivated in, on average, 36% of clear cell renal cell carcinoma (ccRCC). Mutations of BAP1 encode for the histone deubiquitinase BRCA1 associated protein-1, and are present in 10% of ccRCCs. They are largely mutually exclusive with PBRM1 mutations. Mutations to SETD2, a histone methyltransferase, occur in 10% of ccRCC. BAP1- or SETD2-mutated ccRCCs have been associated with poor overall survival, while PBRM1 mutations seem to identify a favorable group of ccRCC tumors. This review describes the roles of PBRM1, BAP1 and SETD2 in the development and progression of ccRCC and their potential for future personalized approaches.

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Section: Bap1mentioning

confidence: 98%

BAP1,PBRM1andSETD2in clear-cell renal cell carcinoma: molecular diagnostics and possible targets for personalized therapies

Piva¹,

Santoni

Matrana

et al. 2015

Expert Review of Molecular Diagnostics

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“…This ubiquitylation is essential for the tumour-suppressing function of BRCA1 in response to DNA damage, and for the radiation-induced loss [Au:OK?] of BAP1-sensitized cells 170 . In addition to its essential role in the orchestrated regulation of the BRCA1-mediated DNA damage response, BAP1 directly deubiquinates H2A119K and binds to E2F family member transcription factors and E2F-responsive promoters.…”

Section: Bap1mentioning

confidence: 99%

The epigenetic landscape of renal cancer

2016

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| The majority of kidney cancers are associated with mutations in the von Hippel-Lindau gene and a small proportion are associated with infrequent mutations in other well characterized tumour-suppressor genes. In the past 15 years, efforts to uncover other key genes involved in renal cancer have identified many genes that are dysregulated or silenced via epigenetic mechanisms, mainly through methylation of promoter CpG islands or dysregulation of specific microRNAs. In addition, the advent of next-generation sequencing has led to the identification of several novel genes that are mutated in renal cancer, such as PBRM1, BAP1 and SETD2, which are all involved in histone modification and nucleosome and chromatin remodelling. In this Review, we discuss how altered DNA methylation, microRNA dysregulation and mutations in histone-modifying enzymes disrupt cellular pathways in renal cancers.

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“…Among the substrates of BAP1, there is the repressive transcriptional regulator host cell factor 1 (HCF1) that acts on E2F-responsive promoters [205]. BAP1 also controls transcription and chromatin structure via histone H2A deubiquitylation [206] and through its interaction with HCF1 and the transcription factor Yin Yang 1 (YY1) affecting the transcription of many genes [207, 208]. Consistent with the profound effect on the transcription profile of the cells, depletion of BAP1 determines cell dedifferentiation and the acquisition of stem cell features [209].…”

Section: Genetics Of Uveal Melanomamentioning

confidence: 99%

The biology of uveal melanoma

Amaro

Gangemi

Piaggio

et al. 2017

Cancer Metastasis Rev

192

193

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Uveal melanoma (UM), a rare cancer of the eye, is distinct from cutaneous melanoma by its etiology, the mutation frequency and profile, and its clinical behavior including resistance to targeted therapy and immune checkpoint blockers. Primary disease is efficiently controlled by surgery or radiation therapy, but about half of UMs develop distant metastasis mostly to the liver. Survival of patients with metastasis is below 1 year and has not improved in decades. Recent years have brought a deep understanding of UM biology characterized by initiating mutations in the G proteins GNAQ and GNA11. Cytogenetic alterations, in particular monosomy of chromosome 3 and amplification of the long arm of chromosome 8, and mutation of the BRCA1-associated protein 1, BAP1, a tumor suppressor gene, or the splicing factor SF3B1 determine UM metastasis. Cytogenetic and molecular profiling allow for a very precise prognostication that is still not matched by efficacious adjuvant therapies. G protein signaling has been shown to activate the YAP/TAZ pathway independent of HIPPO, and conventional signaling via the mitogen-activated kinase pathway probably also contributes to UM development and progression. Several lines of evidence indicate that inflammation and macrophages play a pro-tumor role in UM and in its hepatic metastases. UM cells benefit from the immune privilege in the eye and may adopt several mechanisms involved in this privilege for tumor escape that act even after leaving the niche. Here, we review the current knowledge of the biology of UM and discuss recent approaches to UM treatment.

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BAP1 regulates cell cycle progression through E2F1 target genes and mediates transcriptional silencing via H2A monoubiquitination in uveal melanoma cells

Cited by 51 publications

References 37 publications

BAP1,PBRM1andSETD2in clear-cell renal cell carcinoma: molecular diagnostics and possible targets for personalized therapies

BAP1,PBRM1andSETD2in clear-cell renal cell carcinoma: molecular diagnostics and possible targets for personalized therapies

The epigenetic landscape of renal cancer

The biology of uveal melanoma

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