Scientists Link METTL13 to Tumor Growth Pathway
St. Jude researchers found that methylation of the translation factor eEF1A affects how cells decode messenger RNA, with implications for KRAS-driven cancers.
Updated on Nov. 3, 2026 in Life Sciences

St. Jude Children's Research Hospital scientists identified how the translation factor eEF1A is altered by METTL13 methylation at lysine 55, forming eEF1AK55me2. The findings, published in Nature Cell Biology on November 3, 2026, show the modification promotes efficient translation of codons enriched in oncogenes such as KRAS.
Why it matters
The work points to a potential target for inhibiting KRAS production in tumors, a pathway of interest because KRAS drives many cancer types and can develop treatment resistance. Researchers also observed that tumors resistant to KRAS inhibitors grew more slowly in animal models when METTL13 was disrupted.
The study relied on cell lines lacking METTL13 and single-molecule imaging, with knockout models showing no toxicity in healthy pre-clinical subjects. Patient data correlating higher METTL13 methyltransferase activity with poor prognosis in lung and pancreatic cancers remains observational, and clinical translation is unconfirmed.
The players
St. Jude Children's Research Hospital
A Memphis, Tennessee-based pediatric research hospital that conducts biomedical research on childhood cancers and other diseases.
The details
The team created cell lines lacking METTL13 and recombinantly expressed eEF1A with and without METTL13-mediated methylation. Parallelized single-molecule imaging showed that eEF1AK55me2 affects mRNA decoding kinetically and structurally, with two related codons decoding at very similar rates when METTL13 is present.
Timeline
November 3, 2026: Findings published in Nature Cell Biology.
2023: St. Jude team published a cryo-EM ribosome structure study in Nature.
Big Picture
This builds on St. Jude's 2023 cryo-EM ribosome structure study published in Nature, moving from structural description of the translation machinery toward how specific modifications steer translation in oncogenic pathways. It reflects a broader research direction in which translation regulation is being examined as a source of cancer-specific vulnerabilities.
The findings are pre-clinical, so no treatment changes for patients are imminent. Any future METTL13-targeted therapy would need clinical trials to establish safety and effectiveness before it could reach patients with KRAS-driven cancers.
The takeaway
Translation regulation is emerging as a source of cancer-specific vulnerabilities, and METTL13 is one candidate that researchers are now testing. Readers should treat these results as early-stage laboratory findings rather than a near-term treatment option.
Further reading
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