# The methyltransferase METTL16 in digestive system cancers: functions and mechanisms

## TL;DR

This review explores the role of METTL16, an m6A methyltransferase, in digestive system cancers, highlighting its potential as a diagnostic and therapeutic target.

## Contribution

The paper systematically summarizes METTL16's oncogenic and tumor-suppressive roles in digestive cancers and their mechanisms.

## Key findings

- METTL16 regulates cancer progression via m6A-dependent and -independent mechanisms.
- It influences cell proliferation, apoptosis, metastasis, and chemotherapy resistance in digestive cancers.
- METTL16 shows potential as a diagnostic, prognostic, and therapeutic target.

## 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.