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Researchers at St. Jude Children's Research Hospital have identified how the enzyme METTL13 fuels the growth of KRAS-driven tumors — and how blocking it could overcome treatment resistance. The study, published in Nature Cell Biology, found that METTL13 boosts production of cancer-promoting proteins like KRAS by altering how genetic instructions are read. In animal models, disrupting METTL13 stunted resistant tumor growth without toxic side effects.
Researchers at St. Jude Children's Research Hospital have cracked open a new angle on one of cancer's most stubborn problems: KRAS-driven treatment resistance. Published in Nature Cell Biology, the study reveals how the enzyme METTL13 modifies a key protein involved in reading genetic instructions (eEF1A), boosting the production of cancer-promoting proteins like KRAS. When METTL13 is active, it methylates eEF1A at a specific site, speeding up the decoding of codons enriched in oncogenes — essentially giving tumors a growth advantage.
The team used single-molecule imaging and proteomic profiling to map this mechanism, then tested what happens when METTL13 is disrupted. In animal models of KRAS-inhibitor-resistant tumors, knocking out METTL13 slowed tumor growth — and crucially, it did so without causing toxic effects in healthy tissue.
Key Takeaways:
Why it matters: KRAS mutations drive some of the deadliest cancers, including pancreatic and lung cancers, and resistance to existing KRAS inhibitors is a major clinical hurdle. This research opens a potential new pathway to overcome that resistance.
