MINI REVIEW article
Front. Immunol.
Sec. Cancer Immunity and Immunotherapy
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1709742
This article is part of the Research TopicEpigenetic Alterations in Tumors and Therapeutic ResistanceView all 5 articles
METTL14 in Tumor Immunity: Epitranscriptomic Regulation and Therapeutic Potential
Provisionally accepted
- 1Suining Central Hospital, Suining, China
- 2City of Hope, Duarte, United States
- 3Department of Gastroenterology, Suining Central Hospital, Suining, China
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Abstract N⁶-methyladenosine (m⁶A) is the most abundant internal RNA modification, orchestrated by writers, erasers, and readers. METTL14, a key component of the m⁶A methyltransferase complex, acts as a structural scaffold that ensures substrate recognition and modification precision. Beyond this canonical role, METTL14 regulates multiple biological processes, including chromatin remodeling, transcriptional activity, and senescence-associated signaling. Recent studies highlight its pivotal function in tumor immunity: METTL14 shapes T cell differentiation, CD8⁺ T cell activation, and the activity of macrophages and NK cells, thereby remodeling the tumor immune microenvironment. Moreover, METTL14 directly modulates immune checkpoint pathways by regulating PD-1 and PD-L1 expression, linking epitranscriptomic control with immune escape and therapeutic resistance. Aberrant METTL14 expression correlates with tumor progression and immune evasion, underscoring its potential as a predictive biomarker and therapeutic target. Targeting METTL14, alone or in combination with immune checkpoint inhibitors, may provide novel strategies to enhance immunotherapy efficacy.
Keywords: METTL14, m⁶A methylase, Tumor Microenvironment, Immune checkpoint, cancer immunotherapy
Received: 20 Sep 2025; Accepted: 01 Oct 2025.
Copyright: © 2025 Li, Jiang, Yuan and Wang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Qiang Wang, wangqiang902497@126.com
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