ArticleFrontiers in cell and developmental biology2022
Elevated levels of the methyltransferase SETD2 causes transcription and alternative splicing changes resulting in oncogenic phenotypes.
Article in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Exploring the AAK1 Phospho-signaling Landscape Through Phospho-centric Co-regulation Network.Cell biochemistry and biophysics · 2026Article
- Molecular signature of SETD2 and m6A modifiers in the pathogenesis of different grades of adult-type diffuse gliomas.Molecular biology reports · 2026Article
- The SETD2 L1609P mutation found in leukemia disrupts methyltransferase activity and reduces histone H3K36 trimethylation.The Journal of biological chemistry · 2026Article
- Multi-omics identification of MBNL2 associated with poor pathological response to neoadjuvant chemoimmunotherapy in lung squamous cell carcinoma.Frontiers in oncology · 2026Article
- Postbiotics Combination Synergises the Antiproliferative Effects of Doxorubicin in Gastric Cancer Cells: A Cellular and Molecular Deep Dive.International journal of molecular sciences · 2025Article
- Article
- Histone lysine methylation modifiers controlled by protein stability.Experimental & molecular medicine · 2024Review
- Tumor-suppressive functions of protein lysine methyltransferases.Experimental & molecular medicine · 2023Review
- Structure and Function of RhoBTB1 Required for Substrate Specificity and Cullin-3 Ubiquitination.Function (Oxford, England) · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The methyltransferase SETD2 regulates cryptic transcription, alternative splicing, and the DNA damage response. It is mutated in a variety of cancers and is believed to be a tumor suppressor. Counterintuitively, despite its important role, SETD2 is robustly degraded by the proteasome keeping its levels low. Here we show that SETD2 accumulation results in a non-canonical deposition of the functionally important H3K36me3 histone mark, which includes its reduced enrichment over gene bodies and exons. This perturbed epigenetic landscape is associated with widespread changes in transcription and alternative splicing. Strikingly, contrary to its role as a tumor suppressor, excessive SETD2 results in the upregulation of cell cycle-associated pathways. This is also reflected in phenotypes of increased cell proliferation and migration. Thus, the regulation of SETD2 levels through its proteolysis is important to maintain its appropriate function, which in turn regulates the fidelity of transcription and splicing-related processes.
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