ArticleGenome research2014
Variation in chromatin accessibility in human kidney cancer links H3K36 methyltransferase loss with widespread RNA processing defects.
Article in Genome research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers.
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Who cites it
123 citing papers in PubMed, 186 citations in OpenAlex.
- The Goldilocks state of transcriptional readthrough for chimeric splicing.Transcription · 2026Review
- Aberrant Kupffer-like differentiation of hematopoietic stem cell is critical for the MDS pathogenesis in Setd2-deficient mice.Cell death and differentiation · 2026Article
- Integrated chromatin and transcriptomic profiling reveals sex-specific mechanisms of gene regulation in hepatic nutrient responses.PLoS biology · 2026Article
- Deciphering the interplay between SETD2 mediated H3K36me3 and RNA N6-methyladenosine in clear cell renal cell carcinoma (ccRCC).Epigenetics · 2025Article
- Setd2 ensures the establishment of a precise basal inflammatory state within murine hematopoietic stem/progenitor cells.Cell death & disease · 2025Article
- Emerging role of SETD2 in the development and function of immune cells.Genes & diseases · 2025Review
- SETD2 loss-of-function uniquely sensitizes cells to epigenetic targeting of NSD1-directed H3K36 methylation.Genome biology · 2025Article
- Conserved patterns of transcriptional dysregulation, heterogeneity, and cell states in clear cell kidney cancer.Cell reports · 2025Article
- Prognostic and therapeutic roles ofAging · 2024Article
- Construction and validation of a chromatin regulator-related gene signature for prognostic and therapeutic significance of clear cell renal cell carcinoma.Translational cancer research · 2024Article
- Article
- SETD2 loss in renal epithelial cells drives epithelial-to-mesenchymal transition in a TGF-β-independent manner.Molecular oncology · 2024Article
- Tumor cell-intrinsic SETD2 inactivation sensitizes cancer cells to immune checkpoint blockade through the NR2F1-STAT1 pathway.Journal for immunotherapy of cancer · 2023Article
- The role of histone methylation in renal cell cancer: an update.Molecular biology reports · 2023Review
- SETD2 regulates chromatin accessibility and transcription to suppress lung tumorigenesis.JCI insight · 2023Article
- Alternative Splicing in the Regulatory Circuit of Plant Temperature Response.International journal of molecular sciences · 2023Review
- Histone methyltransferase SETD2: An epigenetic driver in clear cell renal cell carcinoma.Frontiers in oncology · 2023Review
- Adolescent binge ethanol impacts H3K36me3 regulation of synaptic genes.Frontiers in molecular neuroscience · 2023Article
- Stress-induced transcriptional readthrough into neighboring genes is linked to intron retention.iScience · 2022Article
- CHD8 suppression impacts on histone H3 lysine 36 trimethylation and alters RNA alternative splicing.Nucleic acids research · 2022Article
63 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Comprehensive sequencing of human cancers has identified recurrent mutations in genes encoding chromatin regulatory proteins. For clear cell renal cell carcinoma (ccRCC), three of the five commonly mutated genes encode the chromatin regulators PBRM1, SETD2, and BAP1. How these mutations alter the chromatin landscape and transcriptional program in ccRCC or other cancers is not understood. Here, we identified alterations in chromatin organization and transcript profiles associated with mutations in chromatin regulators in a large cohort of primary human kidney tumors. By associating variation in chromatin organization with mutations in SETD2, which encodes the enzyme responsible for H3K36 trimethylation, we found that changes in chromatin accessibility occurred primarily within actively transcribed genes. This increase in chromatin accessibility was linked with widespread alterations in RNA processing, including intron retention and aberrant splicing, affecting ∼25% of all expressed genes. Furthermore, decreased nucleosome occupancy proximal to misspliced exons was observed in tumors lacking H3K36me3. These results directly link mutations in SETD2 to chromatin accessibility changes and RNA processing defects in cancer. Detecting the functional consequences of specific mutations in chromatin regulatory proteins in primary human samples could ultimately inform the therapeutic application of an emerging class of chromatin-targeted compounds.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.