ReviewFrontiers in oncology2026
The methyltransferase METTL16 in digestive system cancers: functions and mechanisms.
Review in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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4 authors.
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Abstract
N6-methyladenosine (m6A) methylation, the most prevalent mRNA modification, affects RNA transcription, splicing, and stability. Methyltransferase-like 16 (METTL16), a novel m6A methyltransferase, regulates the expression of target mRNAs via m6A-mediated modifications. The methyltransferase domain of METTL16 is essential for its catalytic activity. In addition to acting as a methyltransferase, METTL16 can also facilitate mRNA translation in an m6A-independent manner, thus regulating cancer development and progression. Accumulating evidence has indicated that METTL16 plays a pivotal role in the progression of various cancers by regulating cell proliferation, apoptosis, metastasis, and resistance to chemotherapy. In this review, we provide a narrative review of the functions of METTL16 and summarize its oncogenic and tumor-suppressive functions as well as its underlying mechanisms in human digestive system cancers. However, further in-depth studies are required to validate these findings. By comprehensively summarizing the current literature on METTL16, we provide a theoretical basis for its application as a diagnostic and prognostic marker as well as a potential therapeutic target for digestive system cancers.
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