METTL5

Last update 08 May 2025

Basic Info

Synonyms

HSPC133, methyltransferase 5, N6-adenosine, Methyltransferase-like protein 5

+ [2]

Introduction

Catalytic subunit of a heterodimer with TRMT112, which specifically methylates the 6th position of adenine in position 1832 of 18S rRNA (PubMed:31328227, PubMed:32217665, PubMed:33357433, PubMed:33428944, PubMed:35033535). N6-methylation of adenine(1832) in 18S rRNA resides in the decoding center of 18S rRNA and is required for translation and embryonic stem cells (ESCs) pluripotency and differentiation (PubMed:33357433).

100 Clinical Results associated with METTL5

100 Translational Medicine associated with METTL5

0 Patents (Medical) associated with METTL5

Literatures (Medical) associated with METTL5

01 Dec 2025·Molecular Biology Reports

Potential prognostic and predictive biomarkers: METTL5, METTL7A, and METTL7B expression in gastrointestinal cancers

Article

Author: Heydari, Soraya ; Hashemi, Mehrdad ; Ghaedi, Kamran ; Peymani, Maryam ; Entezari, Maliheh

BACKGROUNDThe methyltransferase gene family is known for its diverse biological functions and critical role in tumorigenesis. This study aimed to identify these family genes in common gastrointestinal (GI) cancers using comprehensive methodologies.METHODSGene identification involved analysis of scientific literature and insights from The Cancer Genome Atlas (TCGA) database. RNA sequencing (RNA-seq) data for colon, gastric, pancreatic, esophageal, and liver cancers were collected, processed, and normalized. Differential expression analysis was conducted using R software with the Limma package. Additionally, real-time PCR analysis was performed on 30 tumor and 30 normal tissue samples from patients with colon and gastric cancer. Pathway analysis was conducted via the EnrichR web tool, while survival analysis used Cox regression methods, and biomarker potential was assessed with the pROC package. Prognostic significance was evaluated by examining associations between gene expression, patient survival, and recurrence rates. The study also investigated diagnostic potential through receiver operating characteristic (ROC) analysis, and assessed how small molecules affect gene expression, with implications for drug resistance and sensitivity, analyzed via CCLE and GDSC datasets.RESULTSFindings revealed METTL5 overexpression in colon, liver, esophagus, and pancreas cancers, while METTL7A was underexpressed in gastric, esophagus, liver, and colon cancers. METTL7B expression varied, being higher in gastric and esophagus cancers but lower in liver and colon cancers. Enrichment analysis identified pathways related to these genes, and survival analysis associated altered METTL7A and METTL5 expressions with poor prognosis and higher recurrence rates.CONCLUSIONSThese findings suggest that METTL genes could serve as predictive biomarkers in GI cancers, offering potential implications for patient prognosis and treatment response.

01 Jul 2025·Cellular Signalling

Modulation of Mettl5 alleviates airway allergy by regulating the epigenetic profile of M2 macrophages

Article

Author: Liu, Xiaoyu ; Dong, Yixuan ; Yang, Gui ; Yang, Pingchang ; Liu, Yu ; Geng, Xiaorui ; Liu, Jiangqi ; Liao, Yun ; Zheng, Haoyue ; Liu, Zhiqiang ; Zhang, Xiwen

M2 macrophages (M2 cells) are known to be involved in both Th2 responses and immune regulation. However, the underlying mechanisms remain unclear. Functional abnormalities in macrophages are associated with airway allergy (AA). The objective of this study was to investigate the role of methyltransferase-like 5 (Mettl5) in macrophages and its potential to alleviate AA. In this study, an airway allergy (AA) mouse model was established using dust mite extracts (DME) as the specific antigen. M2 cells were collected from mice with and without AA. The role of Mettl5 in modulating the immune activities of M2 cells was assessed using both epigenetic and immunological approaches. We found that Mettl5 levels were elevated in airway M2 cells from mice with AA. The presence of Mettl5 in airway M2 cells was positively correlated with airway Th2 polarization in these mice. Airway M2 cells from AA mice exhibited impaired immune-suppressive function, which was resolved by ablating the Mettl5 gene in macrophages. Mettl5 was responsible for the hypermethylation of the Il10 promoter in airway M2 cells of AA mice. Exposure to DME induced Mettl5, which in turn recruited USP21 to deubiquitinate GATA3, thereby boosting IL-4 expression in M2 cells. Inhibiting Mettl5 restored the immune-suppressive capacity of airway M2 cells and mitigated experimental AA. In conclusion, Mettl5 plays a critical role in subverting the immune-regulatory capacity and enhancing IL-4 expression in M2 cells. Inhibition of Mettl5 can mitigate experimental AA by restoring the immune-regulatory functions of M2 cells.

01 Feb 2025·Journal of Oral Pathology & Medicine

METTL5 Promotes Tumor Progression in Oral Squamous Cell Carcinoma by Activating the Myc Pathway

Article

Author: Huang, Rong ; Zhang, Shuangyue ; Wang, Ying ; Feng, Xingyu ; Lu, Jiajing ; Zhang, Wei ; Zhou, Tao

ABSTRACTBackgroundIt has been observed that methyltransferases‐like 5 (METTL5) is a key mediator underlying tumorigenesis in humans. This study aimed to investigate the biological function, expression pattern, and clinical significance of METTL5 in oral squamous cell carcinoma (OSCC).MethodsBioinformatics interrogations and immunohistochemical staining were utilized for determining the expression and localization of METTL5 in OSCC, and revealing the relationship between the expression of METTL5 and prognosis. Cell phenotype experiments and xenograft models were used to detect the impact of METTL5 silencing on OSCC. Gene Set Enrichment Analysis, Spearman correlation, and c‐Myc overexpression plasmid was utilized for exploring the regulatory effects of METTL5 on the Myc pathway.ResultsMETTL5 was overexpressed in OSCC and correlated with reduced survival. Cell proliferation, migration, and invasion were significantly inhibited by METTL5 knockdown in vitro, and tumor growth was impaired in vivo. Moreover, METTL5 was capable of activating the Myc pathway. The influences of knockdown of METTL5 on Cal27 cell biological behaviors were reversed by overexpression of c‐Myc.ConclusionsOur data suggested that METTL5 may act as a putative oncogene and prognostic biomarker in OSCC. The Myc pathway appears to be involved in cell proliferation, migration, invasion, and apoptosis in OSCC mediated by METTL5.

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METTL5

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