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Updated: Dec 6, 2025

A Method for Measuring RNA N6-methyladenosine Modifications in Cells and Tissues
Published on: December 5, 2016
SETD2 as a regulator of N6-methyladenosine RNA methylation and modifiers in cancer
Subhadra Kumari1, Srinivasan Muthusamy
1Department of Life Science, National Institute of Technology, Rourkela, India.
Abstract:
Cancer is an unpleasant, painful disease. It is one of the most devastating diseases worldwide diminishing many lives. Many genetic and epigenetic changes occur before cancer develops. Mutation in SETD2 gene is one such example. RNA splicing, DNA damage repair, DNA methylation and histone methylation are some of the biological processes mediated by SETD2. SETD2 (histone H3 lysine 36 methyltransferase) is a frequently mutated gene in different types of cancer. Loss of SETD2 is associated with worse prognosis and aggressive phenotypes. Histone modification is one of the epigenetic regulation having a significant effect on gene regulation. N6-methyladenosine (m6A) mRNA modification is a well-known posttranscriptional modification playing a pivotal role in many normal and pathological processes affecting RNA metabolism. SETD2 catalyses H3K36 trimethylation and in turn H3K36me3 guides the deposition of m6A on nascent RNA transcripts. Finally, this review summarizes the deep understanding of the role of SETD2 in RNA methylation/modification and how SETD2 mutation contributes to tumour development.
Insights
Mutations in the SETD2 gene impact cancer development by altering RNA methylation. Loss of SETD2 function is linked to aggressive cancer phenotypes and worse patient prognosis.
Area of Science:
- Oncology
- Epigenetics
- Molecular Biology
Background:
- Cancer involves genetic and epigenetic alterations.
- SETD2 gene mutations are common in various cancers.
- SETD2 plays roles in RNA splicing, DNA repair, and methylation.
Purpose of the Study:
- To review the role of SETD2 in RNA methylation and modification.
- To elucidate how SETD2 mutations contribute to tumor development.
Main Methods:
- Literature review of studies on SETD2 function and cancer.
- Analysis of the link between SETD2, histone modification, and mRNA methylation.
- Examination of the impact of SETD2 mutations on cancer prognosis.
Main Results:
- SETD2 catalyzes H3K36 trimethylation, which guides m6A RNA methylation.
- Loss of SETD2 is associated with aggressive cancer phenotypes and poor prognosis.
- SETD2 mutations disrupt normal RNA metabolism and contribute to tumorigenesis.
Conclusions:
- SETD2 is crucial for epigenetic regulation and RNA metabolism.
- Altered SETD2 function due to mutations significantly impacts cancer progression.
- Understanding SETD2's role offers potential therapeutic targets for cancer treatment.
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