# Study links METTL3 to DNMT1 protein levels in high-grade serous ovarian cancer

- Published: 2026-11-05 18:23 UTC
- Section: Life & Health › Medicine
- Tags: high-grade serous carcinoma, METTL3, METTL14, m6A RNA modification, DNMT1, TNFAIP3, FBXO32, DNA hypomethylation, tumor suppressor genes
- URL: https://realtech.media/news/rt-afab902c3cf905fc40d963c8_study_links_mettl3/

**Authors report that m6A modification by METTL3 enhances DNMT1 translation and silences tumor suppressor genes. Both are proposed as therapeutic targets in HGSC.**

![Study links METTL3 to DNMT1 protein levels in high-grade serous ovarian cancer](https://sgzwpqqelzmajkcubgkl.supabase.co/storage/v1/object/public/rt-media/2026/11/a8f8b9350b6d0c61.jpg)
*Nephron, Wikimedia Commons, CC BY-SA 3.0*

Researchers reported in Science Advances that the RNA methyltransferase METTL3 and the N6-methyladenosine (m6A) RNA modification pathway play an oncogenic role in high-grade serous carcinoma (HGSC), the most lethal subtype of ovarian cancer. [1] The disease is often diagnosed at advanced stages because it progresses without symptoms and has no early detection markers. [1]

Depletion of METTL3 or its binding partner METTL14 impaired proliferation of ovarian cancer cells and tumor progression. [1] According to the authors, m6A deposition enhances translation of the DNA methyltransferase DNMT1, an epigenetic repressor that silences tumor suppressor genes. [1]

Pharmacologic inhibition of DNMT1 led to DNA hypomethylation and higher expression of the tumor suppressors TNFAIP3 and FBXO32. [1] METTL3 depletion also increased expression of these genes. The authors propose that METTL3 sustains tumor growth by maintaining DNMT1 protein levels and repressing anti-tumor pathways, and they regard METTL3-mediated RNA modifications and DNMT1 as potential therapeutic targets in HGSC. [1]

## Sources

1. [Science Advances](https://doi.org/10.1126/sciadv.aec2297)

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Source: RealTech, realtech.media — https://realtech.media/news/rt-afab902c3cf905fc40d963c8_study_links_mettl3/
