ArticleMedical oncology (Northwood, London, England)2023
SETD2 controls m6A modification of transcriptome and regulates the molecular oncogenesis of glioma.
Article in Medical oncology (Northwood, London, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- Molecular signature of SETD2 and m6A modifiers in the pathogenesis of different grades of adult-type diffuse gliomas.Molecular biology reports · 2026Article
- The dual regulatory role of METTL14-mediated mFrontiers in oncology · 2026Review
- Therapy-induced mRNA, rRNA and tRNA methylation alterations confer tolerance phenotype in tumor cells: mechanism and implications.International journal of biological sciences · 2026Review
- SETD2 drives METTL14-mediated mCellular and molecular life sciences : CMLS · 2025Article
- SETD2 and EZH2: Two epigenetic drivers of prostate cancer.Journal of Cancer · 2025Review
- Article
- Emerging Roles and Mechanisms of RNA Modifications in Neurodegenerative Diseases and Glioma.Cells · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
SETD2 is known for its epigenetic regulatory function and a frequently mutated gene in multiple cancers. Recently, it has been inferred that SETD2 regulates m6A mRNA methylation (epitranscriptome) via H3K36me3. The m6A RNA methylation is vital for tumor maintenance, self-renewal, and tumorigenesis. RNA modifications are executed by writers, readers, and erasers. m6A modifiers work along with the molecular cues, H3K36me3, laid down by SETD2. A positive correlation observed between SETD2 and RNA modifiers signifies their direct role in epitranscriptomics. Hence, understanding the epitranscriptomics will provide a new facet for molecular oncogenesis. Glioma is a common, malignant grade IV tumor with limited therapeutic alternatives and a poor prognosis. Yet, its function in glioma is not fully defined. In the present study, thorough investigations were done in the m6A RNA methylation regulators expression, the molecular pathways leading to tumor progression, and their respective outcomes in SETD2-mediated RNA methylation. In vitro analysis reveals that SETD2 knockdown positively affected the oncogenic properties of the glioma cell line and a global reduction in m6A levels in the transcriptome. The reduction of m6A in the transcriptome can be attributed to the decreased expression of METTL3 and METTL14. Therefore, we conclude that SETD2-mediated m6A modifications are crucial for glioma oncogenesis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.