ArticleDiscover oncology2025
Comprehensive analysis of m7G-related genes METTL1 and WDR4 for predicting prognosis and oncogenic functions in prostate cancer.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- Computational prediction of RNA modification site-disease associations: a systematic review.Briefings in bioinformatics · 2026Pooled it
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10 authors.
Funding
Abstract
backgroundProstate cancer is a prominent global health concern, posing a substantial threat to men's well-being and longevity. N-7methylguanosine (m7G) modification orchestrated by a complex involving METTL1 and WDR4, has garnered attention as a post-transcriptional modification with implications in numerous tumor types. Nevertheless, there is a paucity of research addressing potential pivotal roles of METTL1 and WDR4 in driving prostate cancer progression.
methodsWe obtained mRNA expression data for METTL1 and WDR4 from the TCGA and GSEA databases in prostate cancer patients, analyzing their impact on survival and tumor immune microenvironment. GO and KEGG analyses were performed on associated genes. Univariate and multivariate Cox analyses identified METTL1 and WDR4 as independent prognostic factors, leading to a two-gene predictive model that evaluated tumor mutation burden, immune infiltration, and immune function changes. Importantly, we substantiated the impact of METTL1 and WDR4 on prostate cancer development in vitro.
resultsIn prostate cancer, high METTL1 and WDR4 expression correlated with reduced overall survival and increased plasmacytoid dendritic cells, with decreased adaptive immune cells. Functional enrichment analysis indicated their influence on ribosome-related functions. Our model revealed critical mutation sites and immune infiltration alterations. In vitro, METTL1 or WDR4 knockdown inhibited prostate cancer cell proliferation, migration, and invasion.
conclusionOur study unveils the oncogenic roles of both METTL1 and WDR4 in prostate cancer development. Additionally, the prognostic model founded on METTL1 and WDR4 exhibits enhanced predictive precision for OS, thereby serving as a valuable clinical tool for prostate cancer.
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