ArticleCells2025
The Impact of TRPM8 on Prostate Cancer Transcriptomic Dynamics.
Article in Cells, 2025. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Targeting the nervous system: Mechanistic insights into neuro-tumor communication and therapeutic opportunities.Acta pharmaceutica Sinica. B · 2026Review
- Rewiring melanoma cell fate: TRPM8 modulators trigger apoptosis and boost NK cell cytotoxicity.Cell death & disease · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Prostate cancer (PC) remains a significant health challenge, with androgen receptor (AR) signaling playing a pivotal role in its progression. This study investigates the expression and functional implications of the transient receptor potential melastatin 8 (TRPM8) channel in PC, focusing on its interaction with AR and its impact on oncogenic pathways. We analyzed mRNA expression levels of TRPM8 and AR in PC tissues, revealing that TRPM8 is upregulated in benign and early-stage tumors but significantly downregulated in metastatic samples. This decline correlates with increased AR expression, suggesting a compensatory mechanism that enhances AR-driven tumorigenesis. RNA sequencing and pathway enrichment analyses demonstrated that TRPM8 knockout (KO) prostates exhibited significant alterations in gene expression, particularly in pathways related to extracellular matrix (ECM) remodeling, cell proliferation, and survival signaling. Notably, genes associated with metastasis, such as MMP2 and FAP, were upregulated in TRPM8 KO samples, indicating a potential role for TRPM8 in inhibiting tumor invasion. Furthermore, Gene Set Enrichment Analysis (GSEA) revealed positive enrichment of androgen response, angiogenesis, and epithelial-mesenchymal transition (EMT) pathways in TRPM8 KO prostates, reinforcing the notion that TRPM8 loss creates a pro-tumorigenic environment. Our findings suggest that TRPM8 functions as a molecular brake on PC progression, and its loss may contribute to the development of aggressive disease phenotypes. This study underscores the importance of TRPM8 as a potential therapeutic target and biomarker in PC, warranting further investigation into its role in cancer biology and treatment response.
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Registered trials
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 OpenQuestion graph.