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Integrated Genetic and Proteomic Analysis Identifies PLK1 as a Candidate Therapeutic Target for SETD2-Deficient Clear Cell Renal Cell Carcinoma

ABSTRACT: We systematically analyzed the alterations in histone epigenetic marks (H3K36me3 and H4K16ac), mRNA transcriptome evoked by SETD2 depletion.

ORGANISM(S): Homo sapiens

PROVIDER: GSE107391 | GEO | 2018/11/22

REPOSITORIES: GEO

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Integrated Genetic and Proteomic Analysis Identifies PLK1 as a Candidate Therapeutic Target for SETD2-Deficient Clear Cell Renal Cell Carcinoma

Project description:Integrated Genetic and Proteomic Analysis Identifies PLK1 as a Candidate Therapeutic Target for SETD2-Deficient Clear Cell Renal Cell Carcinoma

| PRJNA419954 | ENA

Profiling of Histone H3 Trimethylation at Lysine 36 (H3K36me3) in HepG2 cells: SETD2 knockdown and control cells

Project description:SETD2 is the specific methyltransferase of H3K36me3. To obtain SETD2-dependent landscape of H3K36me3 in human genome, we performed ChIP sequencing in SETD2 silenced and control HepG2 cells.

2019-02-21 | GSE110318 | GEO

setd2 knockout zebrafish is survivable and fertile: differential and developmental-stress-related requirements for Setd2 and histone H3K36 trimethylation in different vertebrate animals

Project description:Setd2 is the only enzyme that catalyzes histone H3 lysine 36 trimethylation (H3K36me3) on virtually all actively transcribed protein-coding genes, and this mechanism is evolutionarily conserved from yeast to human. Setd2 and H3K36me3 have been revealed to be involved in many important biochemical mechanisms, including DNA repair, alternative mRNA splicing and transcription elongation. However, physiological function of Setd2 in the context of zebrafish development remains elusive. Here we generated zebrafish setd2 mutant lines through disrupting the majority of the protein. And mRNA profiles of wild-type (WT), Setd2(+/-) and Setd2(-/-) zebrafish embryos at 36hpf were generated by deep sequencing, providing an opportunity to uncover molecular programs and functions of Setd2.

2020-05-27 | GSE151238 | GEO

Profiling of N6-methyladenosine in mouse embryonic stem cells: Setd2 knockdown and control cells

Project description:Setd2 is the specific methyltransferase of H3K36me3. To understand the global effect of H3K36me3 on m6A modification, we used mouse embryonic stem cells (mESCs) model with doxycycline (Dox)-induced Setd2 knockdown, and performed m6A-IP followed by sequencing in mESCs with or without Dox treatment. We found that depletion of H3K36me3 by Setd2 silencing globally reduced m6A in mouse transcriptome.

2019-02-21 | GSE110322 | GEO

Dynamic Reprogramming of DNA Methylation in SETD2-Deregulated Renal Cell Carcinoma

Project description:Clear cell renal cell carcinomas (ccRCCs) harbor frequent mutations in epigenetic modifiers including SETD2, the writer for H3K36me3. We profiles DNA methylation across cell line models of SETD2 inactivation and SETD2 mutated primary tumors as this epigenetic mark is linked to H3K36me3 and is a targetable mark for cancer therapy. SETD2 depleted cell line models (long-term and acute) exhibited a hypermethylation phenotype coinciding with ectopic gains in H3K36me3 centered across intergenic regions adjacent to low expression genes that became upregulated with dysregulation of the epigenome. Poised enhancers of developmental genes demonstrated enrichment for the hypermethylation phenotype. Deregulation of the epigenome observed in the cell line models was recapitulated in SETD2 mutated primary ccRCC, papillary renal cell carcinomas, and lung adenocarcinomas.

2015-09-30 | GSE70645 | GEO

Profiling of N6-methyladenosine in HepG2 cells: SETD2, METTL3, METTL14 or WTAP knockdown and control cells

Project description:SETD2 is the specific methyltransferase of H3K36me3, while METTL3, METTL14 and WTAP are the components of m6A methyltransferase complex. To understand the global effect of H3K36me3 on m6A modification, we compared the m6A profiling in SETD2 and METTL3, METTL14 or WTAP knockdown HepG2 cells, and found depletion of H3K36me3 by SETD2 silencing globally reduced m6A in human transcriptome. What’s more, most of the SETD2-dependent hypomethylation sites also responded to knockdown of METTL3, METTL14, or WTAP.

2019-02-21 | GSE110320 | GEO

Loss of Setd2 promote Kras-induced acinar-to-ductal metaplasia and epitheliamesenchymal transition during pancreatic carcinogenesis

Project description:TCGA(PAAD) public database and PDAC tissue array with SETD2/H3K36me3 staining was used to investigate the clinical relevance of SETD2 in PDAC. Furthermore, to define the role of SETD2 in the carcinogenesis of PDAC, we crossed conditional Setd2 knockout mice (PdxcreSetd2flox/flox) together with with KrasG12D mice. Moreover, to examine the role of SETD2 after ductal metaplasia, Crisp/cas9 was used to deplete Setd2 in PDAC cells. RNA-seq and H3K36me3 Chip-seq were performed to uncover the mechanism.

2020-08-02 | GSE126302 | GEO

Profiling of Histone H3 Trimethylation at Lysine 36 (H3K36me3) in mouse embryonic stem cells: Setd2 knockdown and control cells

Project description:Setd2 is the specific methyltransferase of H3K36me3. To obtain Setd2-dependent landscape of H3K36me3 in mouse genome, we used mouse embryonic stem cells (mESCs) model with doxycycline (Dox)-induced Setd2 knockdown, and performed ChIP sequencing in mESCs with or without Dox treatment.

2019-02-21 | GSE110321 | GEO

Single-nucleotide resolution profiling of N6-methyladenosine in SETD2 knockdown HepG2 cells [m6A miCLIP-seq]

Project description:To understand the global effect of H3K36me3 on m6A modification, we compared the m6A profiling in SETD2 knockdown and control HepG2 cells by miCLIP-seq, and found the depletion of H3K36me3 by SETD2 silencing globally reduced m6A in the human transcriptome.

2019-02-21 | GSE121942 | GEO

Splicing enhances recruitment of methyltransferase HYPB/Setd2 and methylation of histone H3 lysine 36

Project description:Several lines of recent evidence support a role for chromatin in splicing regulation. Here we show that splicing can also contribute to histone modification, which implies a bidirectional communication between epigenetics and RNA processing. Genome-wide analysis of histone methylation in human cell lines and mouse primary T cells reveals that intron-containing genes are preferentially marked with H3K36me3 relative to intronless genes. In intron-containing genes, H3K36me3 marking is proportional to transcriptional activity, whereas in intronless genes H3K36me3 is always detected at much lower levels. Furthermore, splicing inhibition impairs recruitment of H3K36 methyltransferase HYPB/Setd2 and reduces H3K36me3, whereas splicing activation has the opposite effect. Moreover, the increase of H3K36me3 correlates with the length of the first intron, consistent with the view that splicing enhances H3 methylation. We propose that splicing is mechanistically coupled to recruitment of HYPB/Setd2 to elongating RNA Polymerase II. This experiment proposes to profile genome-wide binding profiles by ChIP-seq (Illumina, 36 bp tags) of RNA polymerase II (one biological replicate), the histone modification H3K36me3 (2 replicates) and a reference control input sample (genomic DNA after reverse cross-link, one replicate) in a human H1299 lung carcinoma cell line *** Raw data not provided for Samples GSM766322-GSM766324.

2011-07-25 | E-GEOD-30902 | biostudies-arrayexpress

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