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SETD2 loss in renal epithelial cells drives epithelial to mesenchymal transition in a TGFβ-independent manner [ChIP-Seq]

ABSTRACT: SETD2 is one of most frequently mutated genes in renal cell carcinoma. It is generally known as the only histone methyltransferase that catalyze the trimethylation of lysine 36 on histone H3 (H3K36me3). Mutation of this gene and/or loss of its mark have been linked to metastasis and worse patient outcomes in kidney cancer. In this paper, we will examine the mechanism by which SETD2 loss induces epithelial-to-mesenchymal transition (EMT), which is a major pathway that drives invasion and early metastasis in various cancer types. To achieve the goals, we performed several omics analysis including RNA-seq, ChIP-seq and ATAC-seq to characterize how SETD2 deletion alters transcriptome and epigenome.

ORGANISM(S): Homo sapiens

PROVIDER: GSE213257 | GEO | 2023/07/12

REPOSITORIES: GEO

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SETD2 loss in renal epithelial cells drives epithelial to mesenchymal transition in a TGFβ-independent manner [RNA-Seq]

Project description:SETD2 is one of most frequently mutated genes in renal cell carcinoma. It is generally known as the only histone methyltransferase that catalyze the trimethylation of lysine 36 on histone H3 (H3K36me3). Mutation of this gene and/or loss of its mark have been linked to metastasis and worse patient outcomes in kidney cancer. In this paper, we will examine the mechanism by which SETD2 loss induces epithelial-to-mesenchymal transition (EMT), which is a major pathway that drives invasion and early metastasis in various cancer types. To achieve the goals, we performed several omics analysis including RNA-seq, ChIP-seq and ATAC-seq to characterize how SETD2 deletion alters transcriptome and epigenome.

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SETD2 loss in renal epithelial cells drives epithelial to mesenchymal transition in a TGFβ-independent manner [ATAC-Seq]

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Project description:SETD2, a H3K36 trimethyltransferase, is frequently mutated in human cancers with the highest prevalence (13%) in clear cell renal cell carcinoma (ccRCC). Genomic profiling of primary ccRCC tumors reveals a positive correlation between SETD2 mutations and metastasis. However, whether and how SETD2-loss promotes metastasis remains unclear. Here, we detected SETD2 mutations in 24 of 51 (47%) metastatic ccRCC tumors. Using SETD2-mutant metastatic ccRCC patient-derived cell line and xenograft models, we showed that H3K36me3 restoration greatly reduced distant metastases of ccRCC in mice. An integrated ATAC-seq, ChIP-seq, and transcriptome analysis concluded a tumor suppressor model in which loss of SETD2-mediated H3K36me3 activates enhancers to drive oncogenic transcription through dysregulating histone chaperone recruitment, enhancing histone exchange, and expanding chromatin accessibility. Furthermore, we uncovered mechanism-based therapeutic strategies for SETD2-deficient cancer through inhibition of histone chaperones. Overall, SETD2-loss creates a permissive epigenetic landscape for cooperating oncogenic drivers to amplify transcriptional output, providing unique therapeutic opportunities.

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SETD2 loss in renal epithelial cells drives epithelial to mesenchymal transition in a TGFβ-independent manner [RNA-Seq]

Project description:SETD2 loss in renal epithelial cells drives epithelial to mesenchymal transition in a TGFβ-independent manner [RNA-Seq]

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SETD2 loss in renal epithelial cells drives epithelial to mesenchymal transition in a TGFβ-independent manner [ChIP-Seq]

Project description:SETD2 loss in renal epithelial cells drives epithelial to mesenchymal transition in a TGFβ-independent manner [ChIP-Seq]

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