ArticlePloS one2020
TRPM4 is overexpressed in breast cancer associated with estrogen response and epithelial-mesenchymal transition gene sets.
Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- TRP Channels Interactome as a Novel Therapeutic Target in Breast Cancer.Frontiers in oncology · 2021Pooled it
- Article
- Structural mechanism of Necrocide 1 activation of human TRPM4 that triggers necrosis by sodium overload.Nature communications · 2026Article
- Structural mechanism of Necrocide 1 activation of human TRPM4 that triggers necrosis by sodium overload.bioRxiv : the preprint server for biology · 2026Article
- Comprehensive bioinformatic analysis reveals TRPM4 as a biomarker for pan-cancer progression and macrophage infiltration.Discover oncology · 2026Article
- TRPM4 expression predicts prognosis and modulates the immune microenvironment in pancreatic adenocarcinoma.Scientific reports · 2025Article
- The TRP channels serving as chemical-to-electrical signal converter.Physiological reviews · 2025Review
- Single Dose of a Small Molecule Leads to Complete Regressions of Large Breast Tumors in Mice.ACS central science · 2025Article
- TRPM6 acts as a prognostic biomarker and mediates MgFrontiers in immunology · 2025Article
- Photodiagnosis and photodynamic recognition of cervical cancer with SEM and AFM images.PloS one · 2025Article
- TRP channels and breast cancer: the role of TRPs in the pathophysiological development.Frontiers in molecular biosciences · 2025Review
- Necrosis by sodium overload-associated genes TRPM4 and SLC9A1: biological roles and clinical implications in breast cancer progression.Frontiers in immunology · 2025Article
- TRPM channels in human cancers: regulatory mechanism and therapeutic prospects.Biomarker research · 2024Review
- Acetalax (Oxyphenisatin Acetate, NSC 59687) and Bisacodyl Cause Oncosis in Triple-Negative Breast Cancer Cell Lines by Poisoning the Ion Exchange Membrane Protein TRPM4.Cancer research communications · 2024Article
- Pan-Cancer Analysis of the TRP Family, Especially TRPV4 and TRPC4, and Its Expression Correlated with Prognosis, Tumor Microenvironment, and Treatment Sensitivity.Biomolecules · 2023Article
- Article
- Calcium-Related Genes Predicting Outcomes and Serving as Therapeutic Targets in Endometrial Cancer.Cells · 2022Article
- Article
- TRPs in Ovarian Serous Cystadenocarcinoma: The Expression Patterns, Prognostic Roles, and Potential Therapeutic Targets.Frontiers in molecular biosciences · 2022Article
- New Insights and Emerging Therapeutic Approaches in Prostate Cancer.Frontiers in endocrinology · 2022Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ion channels form an important class of drug targets in malignancies. Transient receptor potential cation channel subfamily M member 4 (TRPM4) plays oncological roles in various solid tumors. Herein, we examined TRPM4 protein expression profile by immunohistochemistry (IHC) in breast cancer cases compared with normal breast ducts, its association with clinico-demographical parameters, and its potential function in breast cancers by Gene Set Enrichment Analysis (GSEA). Data-mining demonstrated that TRPM4 transcript levels were significantly higher in The Cancer Genome Atlas series of breast cancer cases (n = 1,085) compared with normal breast tissues (n = 112) (p = 1.03 x 10-11). Our IHC findings in tissue microarrays showed that TRPM4 protein was overexpressed in breast cancers (n = 83/99 TRPM4+; 83.8%) compared with normal breast ducts (n = 5/10 TRPM4+; 50%) (p = 0.022). Higher TRPM4 expression (median frequency cut-off) was significantly associated with higher lymph node status (N1-N2 vs N0; p = 0.024) and higher stage (IIb-IIIb vs I-IIa; p = 0.005). GSEA evaluation in three independent gene expression profiling (GEP) datasets of breast cancer cases (GSE54002, n = 417; GSE20685, n = 327; GSE23720, n = 197) demonstrated significant association of TRPM4 transcript expression with estrogen response and epithelial-mesenchymal transition (EMT) gene sets (p<0.01 and false discovery rate<0.05). These gene sets were not enriched in GEP datasets of normal breast epithelium cases (GSE10797, n = 5; GSE9574, n = 15; GSE20437, n = 18). In conclusion, TRPM4 protein expression is upregulated in breast cancers associated with worse clinico-demographical parameters, and TRPM4 potentially regulates estrogen receptor signaling and EMT progression in breast cancer.
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