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Dual roles of RNF2 in melanoma progression [expression]

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 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Kadir Akdemir

PROVIDER: E-GEOD-51928 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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 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

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 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.

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2012-04-28 | E-GEOD-33092 | biostudies-arrayexpress

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

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

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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.

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