ArticleDiscover oncology2026
Comprehensive bioinformatic analysis reveals TRPM4 as a biomarker for pan-cancer progression and macrophage infiltration.
Article in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed.
- Necrosis by Sodium Overload: Mechanisms, Pathophysiological Roles, and Therapeutic Prospects of a Novel Form of Regulated Cell Death.Cell biochemistry and biophysics · 2026Review
- Integrative Machine Learning Framework Revealing TRPM4-Associated Signatures and Identifying SPATA6 as a Potential Biomarker in Prostate Cancer.Journal of Cancer · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundIon channels play key regulatory roles in cancer pathophysiology. They are also considered promising therapeutic targets. The transient receptor potential melastatin 4 (TRPM4) is a nonselective monovalent cation channel, recently identified as critical in necrosis by sodium overload. Multiple studies have demonstrated that this gene is a potential player in cancer biology; however, its comprehensive role in various cancer types remains largely unexplored.
methodsIn this study, we conducted a comprehensive bioinformatics analysis of TRPM4 across multiple cancer types, examining its expression patterns, prognostic significance, and clinical relevance. We investigated epigenetic modifications, the DNA damage repair response, as well as alternative splicing and intronic polyadenylation associated with TRPM4. In addition, we analyzed signaling pathways related to tumorigenesis and immune responses, alongside assessing immune cell infiltration in tumor microenvironments.
resultsWe systematically delineate the expression heterogeneity of TRPM4 across pan-cancer and its clinical implications: it acts as a risk factor indicating poor prognosis in ACC, LGG, PAAD, MESO, and UVM, whereas it exhibits a protective role in KIRP and UCEC. Mechanistically, TRPM4 is involved not only in epigenetic regulation and DNA damage repair responses but also modulates post-transcriptional processes such as alternative splicing and intronic polyadenylation. Furthermore, TRPM4 expression is significantly associated with multiple tumor-related signaling pathways and immunomodulatory molecules. More importantly, through tumor microenvironment infiltration analysis, we observed spatial co-localization of TRPM4 with CD68⁺ tumor-associated macrophages, suggesting that TRPM4 may exert a potential immunomodulatory function by shaping the tumor immune microenvironment through influencing immune cell infiltration.
conclusionOur research highlights TRPM4 as a promising biomarker and a therapeutic target for cancer treatment. Future investigations should focus on elucidating the mechanistic role of TRPM4 in modulating immune response and tumor progression, potentially paving the way for innovative therapeutic strategies in oncology.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.