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Dual roles of RNF2 in melanoma progression [ChIP-seq]

ABSTRACT: Epigenetic regulators have emerged as critical factors governing the biology of cancer. Here, in the context of melanoma, we show that RNF2 is prognostic, exhibiting progression-correlated expression in human melanocytic neoplasms. Through a series of gain of function and loss of function studies, we establish that RNF2 is oncogenic and pro-metastatic. Mechanistically, RNF2-mediated invasive behavior is dependent on its ability to mono-ubiquitinate H2AK119 at the promoter of LTBP2, resulting in silencing of this negative regulator of TGFβ signaling. In contrast, RNF2's oncogenic activity did not require its catalytic activity nor derives from its canonical gene repression function, rather RNF2 drives proliferation through direct transcriptional up-regulation of the cell cycle regulator CCND2. In summary, RNF2 regulates distinct biological processes in the genesis and progression of melanoma via distinct molecular mechanisms, underscoring the complex and multi-faceted actions of epigenetic regulators in cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE51929 | GEO | 2016/01/01

SECONDARY ACCESSION(S): PRJNA229782

REPOSITORIES: GEO

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Dual roles of RNF2 in melanoma progression [ChIP-seq]

Project description:Epigenetic regulators have emerged as critical factors governing the biology of cancer. Here, in the context of melanoma, we show that RNF2 is prognostic, exhibiting progression-correlated expression in human melanocytic neoplasms. Through a series of gain of function and loss of function studies, we establish that RNF2 is oncogenic and pro-metastatic. Mechanistically, RNF2-mediated invasive behavior is dependent on its ability to mono-ubiquitinate H2AK119 at the promoter of LTBP2, resulting in silencing of this negative regulator of TGFÎ² signaling. In contrast, RNF2's oncogenic activity did not require its catalytic activity nor derives from its canonical gene repression function, rather RNF2 drives proliferation through direct transcriptional up-regulation of the cell cycle regulator CCND2. In summary, RNF2 regulates distinct biological processes in the genesis and progression of melanoma via distinct molecular mechanisms, underscoring the complex and multi-faceted actions of epigenetic regulators in cancer. RNF2 is overexpressed in immortalized human melanocytes HMEL-BRAFV600E to address impact of RNF2 overexpression in melanoma and identify RNF2 target genes. ChIP was performed to identify RNF2 binding sites using antibody against the V5 tag.

2016-07-03 | E-GEOD-51929 | biostudies-arrayexpress

Dual roles of RNF2 in melanoma progression [expression]

Project description:Epigenetic regulators have emerged as critical factors governing the biology of cancer. Here, in the context of melanoma, we show that RNF2 is prognostic, exhibiting progression-correlated expression in human melanocytic neoplasms. Through a series of gain of function and loss of function studies, we establish that RNF2 is oncogenic and pro-metastatic. Mechanistically, RNF2-mediated invasive behavior is dependent on its ability to mono-ubiquitinate H2AK119 at the promoter of LTBP2, resulting in silencing of this negative regulator of TGFÎ² signaling. In contrast, RNF2's oncogenic activity did not require its catalytic activity nor derives from its canonical gene repression function, rather RNF2 drives proliferation through direct transcriptional up-regulation of the cell cycle regulator CCND2. In summary, RNF2 regulates distinct biological processes in the genesis and progression of melanoma via distinct molecular mechanisms, underscoring the complex and multi-faceted actions of epigenetic regulators in cancer. RNF2 is overexpressed in immortalized human melanocytes HMEL-BRAFV600E to address impact of RNF2 overexpression in melanoma. GFP was overexpressed in HMEL-BRAFV600E cells as a control cell line. Expression profiling using microarray was performed and compared between RNF2 overexpressing versus GFP overexpressing HMEL-BRAFV600E cells.

2016-07-03 | E-GEOD-51928 | biostudies-arrayexpress

Dual roles of RNF2 in melanoma progression [expression]

Project description:Epigenetic regulators have emerged as critical factors governing the biology of cancer. Here, in the context of melanoma, we show that RNF2 is prognostic, exhibiting progression-correlated expression in human melanocytic neoplasms. Through a series of gain of function and loss of function studies, we establish that RNF2 is oncogenic and pro-metastatic. Mechanistically, RNF2-mediated invasive behavior is dependent on its ability to mono-ubiquitinate H2AK119 at the promoter of LTBP2, resulting in silencing of this negative regulator of TGFβ signaling. In contrast, RNF2's oncogenic activity did not require its catalytic activity nor derives from its canonical gene repression function, rather RNF2 drives proliferation through direct transcriptional up-regulation of the cell cycle regulator CCND2. In summary, RNF2 regulates distinct biological processes in the genesis and progression of melanoma via distinct molecular mechanisms, underscoring the complex and multi-faceted actions of epigenetic regulators in cancer.

2016-01-01 | GSE51928 | GEO

LFQMS of RING2 (RING1B, RNF2) immunoprecipitation from MDA-MB-231 and T47D breast cancer cells

Project description:Polycomb repressive complex PRC1 is essential for gene regulation in numerous cell fate decisions. We show that RING1B (RING2, RNF2) and canonical PRC1 (cPRC1) genes are amplified and overexpressed in breast cancer (BC). Moreover, cPRC1 complexes functionally associate with genes regulated by cell type specific key transcription factors such as estrogen receptor (ER) in ER+ tumor cells and BRD4 in triple negative BC cells. cPRC1 is recruited to active enhancers in a manner independent of PRC2 and RING1B enzymatic activity. RING1B regulates enhancer activity and gene transcription not only by promoting the expression of BC oncogenes but also by regulating chromatin accessibility for oncogenic transcription factors. RING1B recruitment, and thus PRC1 association, to active enhancers occurs in multiple cancers.

2018-10-19 | PXD009570 | Pride

Genome-wide binding of RNF2 in control and GPR17 knock-down U87-MG cells

Project description:GPR17 over-expression inhibits glioma cell proliferation and induces apoptosis by raising ROS levels, and mechanistically inhibits the transcription of RNF2, leading to reduced histone H2A monoubiquitination. Here, To identify the genes mediating the effects of GPR17 and RNF2 on ROS level, we performed RNA-Seq of WT and U87-GPR17 cells and RNF2 ChIP-Seq of WT and U87-shGPR17 cells.

2022-05-10 | GSE174121 | GEO

The Polycomb Group protein Rnf2/Ring1b is essential for zebrafish development and cardiogenesis

Project description:Goal of the experiment was to assess the differences in gene expression between zygotic rnf2 mutant zebrafish embryos and wildtype embryos at 3 dpf. The goal of ChIP-sequencing of wildtype embryos at 3 dpf is to link deregulation in gene expression to the Rnf2 occupancy in the wildtype situation and check the overlap between Rnf2 and H3K27me3. The RNA-sequencing of single hearts was performed to assess differences in gene expression between zygotic rn2 mutants hearts and wildtype hearts at 3 different stages (1, 2, 3 dpf)

2019-03-13 | GSE114038 | GEO

Bap1 and RNF2 ChIP-seq in mES cells

Project description:Malignancies arising from mutation of tumor suppressor genes display an unexplained tissue proclivity. For example, tumor suppressor BAP1 encodes a ubiquitously expressed deubiquitinase for histone H2A but germline mutations predominantly cause uveal melanomas and mesotheliomas. We show that BAP1 inactivation causes apoptosis in mouse embryonic stem cells, fibroblasts, liver and pancreas, whereas melanocytes and mesothelial cells remain viable. E3 ligase RNF2, which silences genes by monoubiquitinating H2A, promoted apoptosis in BAP1-deficient cells by suppressing the pro-survival genes Bcl-2 and Mcl-1. Our data argue that BAP1 modulates gene expression by countering H2A ubiquitination, but its loss only promotes tumorigenesis in cells that do not engage an RNF2-dependent apoptotic program. We propose that intolerance of BAP1 loss, and perhaps the loss of other tumor suppressors, restricts the mutant tumor spectrum.

2019-03-26 | GSE120302 | GEO

Bap1 and RNF2 ChIP-seq in mES cells

Project description:Bap1 and RNF2 ChIP-seq in mES cells

| PRJNA492460 | ENA

The role of the core PRC1 members Ring1 and Rnf2 in expression regulation during oocyte growth

Project description:Comparative expression analysis between germinal vesicle (GV) stage mouse oocytes of Ring1-deficient oocytes ("control") versus oocytes deficient for Ring1 and Rnf2 ("mutant").

2020-05-12 | GSE137030 | GEO

Mdm2 enhances stemness-promoting chromatin modifications through the Polycomb Repressor Complex 2 in a p53-Independent Manner [ChIP-Seq]

Project description:The Mdm2 oncoprotein ubiquitinates and antagonizes p53 but may also carry out p53-independent functions. Here we report that Mdm2 is required for the efficient generation of induced pluripotent stem cells (iPSCs) from murine embryonic fibroblasts, in the absence of p53. Similarly, Mdm2 depletion in the context of p53 deficiency also promoted the differentiation of human mesenchymal stem cells and diminished clonogenic survival of cancer cells. Most of the Mdm2-controlled genes also responded to the inactivation of the Polycomb Repressor Complex 2 (PRC2) and its catalytic component EZH2. Mdm2 physically associated with EZH2 on chromatin, enhancing the trimethylation of Histone 3 at lysine 27 and the ubiquitination of Histone 2A at lysine 119 (H2AK119) at its target genes. Removing Mdm2 simultaneously with the H2AK119 E3 ligase Ring1B/RNF2 further induced these genes and synthetically arrested cell proliferation. In conclusion, Mdm2 supports the Polycomb-mediated repression of lineage specific genes independent of p53. H3K27me3 and H2Ak119ub1 ChIP-Seq

2015-12-31 | E-GEOD-73293 | biostudies-arrayexpress

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