Ask about this productRelated genes to: METTL5 antibody
- Gene:
- METTL5 NIH gene
- Name:
- methyltransferase like 5
- Previous symbol:
- -
- Synonyms:
- HSPC133
- Chromosome:
- 2q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-04-14
- Date modifiied:
- 2014-11-18
Related products to: METTL5 antibody
Related articles to: METTL5 antibody
- N-methyladenosine (mA) RNA methylation is implicated in cancer metabolism; however, to the best of our knowledge, the role of methyltransferase 5 (METTL5) in non-small cell lung cancer (NSCLC) progression remains unclear. Reprogrammed glycolytic metabolism (Warburg effect) supports tumor growth and immune evasion; however, the regulatory mechanisms of this process require further investigation. We hypothesized that METTL5 drives NSCLC progression by regulating glycolytic metabolism through mA modification of phosphoglycerate mutase 1 (PGAM1) mRNA. The present study aimed to elucidate the molecular mechanisms, functional impacts and clinical relevance of the METTL5/PGAM1 axis. Integrated analyses of NSCLC cohorts from The Cancer Genome Atlas database were performed, and models (A549 and PC9 cell lines) and molecular techniques, including methylation inhibition, RNA stability assays and metabolic flux measurements (Seahorse XFe96 analyzer), were used. Key interactions were validated through western blotting, reverse transcription-quantitative PCR and correlation analyses. METTL5 was significantly upregulated in NSCLC tissues and in A549, PC9 and H520 cell lines, and high METTL5 expression was associated with poor patient survival (P<0.05). Silencing of METTL5 suppressed NSCLC cell proliferation and migration, while overexpression promoted proliferation and migration. METTL5 directly targeted PGAM1 mRNA through mA modification, and the expression levels of METTL5 and PGAM1 exhibited a statistically significant but moderate positive correlation (R=0.45; P=5.4×10). YTH N-methyladenosine RNA binding protein 1 (YTHDF1) is an m6A reader that recognizes and binds to methylated PGAM1 mRNA, enhancing its stability and expression. PGAM1 knockdown reduced glycolysis (decreased extracellular acidification rate) and increased oxidative phosphorylation (increased oxygen consumption rate). Notably, the positive correlation between PGAM1 and GLUT1 expression (R=0.6; P=4.12×10) supports the role of the METTL5/PGAM1 axis in regulating GLUT1, thereby influencing glycolytic flux. Rescue experiments demonstrated that PGAM1 overexpression reversed GLUT1 downregulation in METTL5-knockdown cells. Overall, METTL5 may drive NSCLC progression by reprogramming glycolytic metabolism through mA modification of PGAM1 mRNA. The METTL5/PGAM1/GLUT1 axis represents a novel therapeutic target for NSCLC. - Source: PubMed
Publication date: 2026/04/20
Shan YuchenDuan XiaoyuYuan KaiLou MingWu QiyongGao Zhaojia - Oral squamous cell carcinoma (OSCC) is a malignant tumour with high-local invasiveness and lymph node metastasis potential. It is associated with poor prognosis and postoperative cosmetic complications. Therefore, developing molecular targets for early detection, diagnosis, and treatment is imperative. Methyltransferase-like 5 (METTL5), a newly identified N6-methyladenosine (m6A) modification writer, has been shown to exhibit tumour-promoting functions in several cancers. However, the significance of METTL5 expression in OSCC remains unexplored. - Source: PubMed
Publication date: 2026/04/21
Kajiya YukaShima KaoriShimojukkoku YudaiOku YasunobuTsuchiyama TakahiroHigashimoto KanakoKurihara-Shimomura MiyakoSasahira Tomonori - - Source: PubMed
Publication date: 2026/04/16
Ji TaoMiao XiangzhuoFang YinghaoNie JianminZhu QingZhu PengyuLiao WeiYang Dinghua - Biallelic pathogenic variants in METTL5, which encodes an RNA methyltransferase involved in the m6A modification of 18S rRNA, have been reported as a rare etiology of autosomal recessive intellectual disability (ID). However, However, the clinical relevance of heterozygous variants in this gene remains unclear. In this study, we report a heterozygous frameshift variant located in exon 1 of the METTL5 gene identified in a father and son presenting with ID. Functional analyses demonstrated that this variant abolishes conserved domains, markedly reduces protein expression, and impairs 18S rRNA m6A modification, accompanied by decreased global protein synthesis. Proteomic profiling further revealed a downregulation of neuronal proteins involved in neuron projection, providing biological evidence supporting a potential role of METTL5 haploinsufficiency in neurodevelopmental processes. These observations suggest that heterozygous loss-of-function variants in METTL5, particularly those occurring early in the coding sequence, may be associated with an increased risk of neurodevelopmental disorders. Taken together, our study expands the mutational and phenotypic spectrum of METTL5-related disorders. - Source: PubMed
Tao WenjunYing YanqinSun JiajuWu YuxinJiang XinhuiZhang JunZhou Jun - Traumatic brain injury (TBI) is a major global health issue leading to high mortality and disability. Activated astrocytes are one of the pivotal driving factors in the neuroinflammatory cascade following TBI. This study aims to investigate the role of esketamine on TBI and the underlying mechanism. Mice received a mouse weight-drop cortical impact or sham surgery and TBI mice were treated with either vehicle or esketamine at 2 h post-injury for 7 consecutive days. The modified Neurological Severity Scoring system, Rotarod test, Open Field test and Novel Object Recognition test were used to assess the neurological function after TBI. And cortical tissues surrounding focal trauma were obtained for Nissl staining, immunofluorescence, ELISA assay and western blotting. In vitro, astrocytes were induced with LPS, followed by the addition of esketamine to the culture medium. After a 24 h exposure, the astrocytes were collected for CCK-8 assay, qRT-PCR, western blotting, immunofluorescence and Co-IP analysis. Esketamine dramatically improved the neurological outcome of mice and reduced neuronal cell death (P < 0.05) and neuroinflammation after TBI. Its anti-inflammatory benefits stem from its ability to suppress astrocyte activation (P < 0.05), inhibit pro-inflammatory A1 astrocyte differentiation (P < 0.01), and promote the formation of protective A2 astrocytes (P < 0.01). Esketamine exerts its effects by inhibiting the METTL5/c-Myc/PD-L1 signaling pathway. Esketamine can effectively alleviate activated astrocytes and promote the polarization of activated astrocytes toward A2 following TBI by inhibiting the METTL5/c-Myc/PD-L1, demonstrating significant anti-inflammatory and neuroprotective effects. - Source: PubMed
Publication date: 2026/03/13
Luo LanYu MiaoLi XiaoyanBi YonghongDuan PengyuMeng YaoJin ZhehaoFeng WeiyuLi LongfeiXing YulingChen JialiZhang Bing