Unraveling the significance of methyltransferase like-3 in the pathogenesis of gastrointestinal tumors - A review

Sep 22, 2026

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Gastrointestinal cancer remains a major public health threat, driven by high incidence and mortality. N6-methyladenosine (m6A), a pervasive internal RNA modification, is central to gastrointestinal tumor initiation and development. Methyltransferase-like 3 (Mettl3) is highlighted as a key component in forming m6A and may influence cancer progression. Evaluating Mettl3 expression supports its use as a prognostic biomarker, informing patient outcomes and disease trajectory. Mechanistic and clinical clarification of Mettl3 could enable targeted therapies and more personalized treatment approaches.

LanguageEnglish

CategoryHealthcare

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Pages14

Reading Time35 min

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Introduction

® Narrative Review Unraveling the significance of methyltransferase like-3 in the pathogenesis of gastrointestinal tumors A review Luxi Xiong, MMa , Qi Ai, MMa , Caijuan Liu, BDa , Weiwei Yang, BDa , Logen Liu, MDb ,c , Guo-Qing Li, MDa ,c ,* | Abstract
In developing countries, gastrointestinal cancer remains a major public health concern due to its high incidence and mortality rates, posing a serious threat to human well-being. N6-methyladenosine, an internal modification found in common eukaryotic RNAs, plays a critical role in the initiation and development of gastrointestinal tumors. Among the key players in N6-methyladenosine formation is methyltransferase-like 3 (Mettl3). This article examines the prognostic implications of Mettl3 expression in gastrointestinal cancers, shedding light on its potential as a biomarker for disease progression and patient outcomes. Understanding the intricate role of Mettl3 in gastrointestinal tumor pathogenesis holds promise for the development of targeted therapies and personalized treatment strategies. Further investigation into the molecular mechanisms and clinical implications of Mettl3 in these cancers will pave the way for more effective interventions and improved patient care in the future. | | --- | | Abbreviations: 5-FU = 5-fluorouracil , ADAMTS9 = ADAM metallopeptidase with thrombospondin type 1 motif 9 , AKT = protein kinase B, ANLN = anillin actin-binding protein, APAF1 = apoptotic protease-activating factor 1, APC = adenomatous polyposis coli, ASPM = abnormal spindle-like microcephaly, DDX23 = DEAD-box helicase 23, EIF3H = factor 3 subunit H, EMT = epithelialmesenchymal transition, ERD = Resina Draconis, ERK = extracellular signal-regulated kinase, FEN1 = Flap endonuclease-1, GLS2 = glutaminase 2, H3K4me3 = histone H3 at lysine 4, HBXIP = hepatitis B x-interacting protein, HCC = hepatocellular carcinoma, HDGF = hepatoma-derived growth factor, HLECs = human lymphatic endothelial cells, IFIT2 = interferon induced protein with tetratricopeptide repeats 2, IGF2BP1 = insulin-like growth factor-2 mRNA-binding protein 1, KLF2 = Krüppel-like factor 2, LDHA = lactate dehydrogenase A, LIFR-AS1 = leukemia inhibitory factor receptor antisense RNA 1, m6A = N6-methyladenosine, MAPK = mitogen-activated protein kinase, Mettl3 = methyltransferase-like 3, MTF1 = metal regulatory transcription factor 1, mTOR = mammalian target of rapamycin, NOTCH1 = notch homolog protein 1, PARP1 = poly[ADP-ribose] polymerase 1, PDAC = pancreatic ductal adenocarcinoma, PD-L1 = programmed death-ligand 1, PI3K = phosphoinositide 3-kinase, PLK1 = polo-like kinase 1, PNN = pinin, PTEN = phosphatase and tensin homolog, SAM = s-adenosylmethionine, SMS = spermine synthase, SOCS2 = suppressor of cytokine signaling 2, SUMO = small ubiquitin-related modifier, TAMs = tumor-associated macrophages, TNFR1 = tumor necrosis factor receptor 1, VEGFA = vascular endothelial growth factor A, WTAP = Wilms’ tumor 1-associated protein, WWP2 = WW domain-containing protein 2, YTHD = YT512-B homology-domain. | | Keywords: biomarker, gastrointestinal cancer, Mettl3 , N6-methyladenosine (m6A) , RNA modification, targeted therapies | 1. Introduction Gastrointestinal cancer comprises a significant proportion of the cancer burden worldwide, accounting for 26% of the global incidence rate and 35% of all cancer-related deaths. Primary malignancies within the gastrointestinal tract include gastric cancer, liver cancer, esophageal cancer, pancreatic cancer, and colorectal cancer.[1] Genetic changes that regulate epigenetic processes have been found to be drivers of cancer, and unlike genetic events, epigenetic changes are reversible.[2] At present, it has been found that many chemical modifications on human RNA are involved in the development of cancer. RNA posttranscriptional This study was supported by grants from the Natural Science Foundation of Hunan province (grant number 2022JJ30517), the Science and Technology Depart

FAQs

Why is methyltransferase-like 3 (Mettl3) considered important in gastrointestinal tumors?

Mettl3 is a key player in forming N6-methyladenosine (m6A), an internal RNA modification linked to tumor initiation and development.

How can Mettl3 expression help clinicians?

Mettl3 expression has prognostic implications, supporting its potential as a biomarker for disease progression and patient outcomes.

What therapeutic direction does the review suggest for Mettl3-related mechanisms?

Understanding Mettl3’s role in gastrointestinal tumor pathogenesis could support development of targeted therapies and personalized treatment strategies.

Sep 22, 2026

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