ArticleOncology letters2018
RNA interference-mediated depletion of TRPM8 enhances the efficacy of epirubicin chemotherapy in prostate cancer LNCaP and PC3 cells.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 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
9 citing papers in PubMed, 12 citations in OpenAlex.
- Rewiring melanoma cell fate: TRPM8 modulators trigger apoptosis and boost NK cell cytotoxicity.Cell death & disease · 2026Article
- Role of TRP Channels in Cancer-Induced Bone Pain.International journal of molecular sciences · 2025Review
- Epirubicin-sensitive detection with a CoWOADMET & DMPK · 2025Article
- TRPM channels in human cancers: regulatory mechanism and therapeutic prospects.Biomarker research · 2024Review
- TRPM8 thermosensation in poikilotherms mediates both skin colour and locomotor performance responses to cold temperature.Communications biology · 2023Article
- Therapeutic potential of TRPM8 channels in cancer treatment.Frontiers in pharmacology · 2023Review
- On the modulation of TRPM channels: Current perspectives and anticancer therapeutic implications.Frontiers in oncology · 2022Review
- Calcium cytotoxicity sensitizes prostate cancer cells to standard-of-care treatments for locally advanced tumors.Cell death & disease · 2020Article
- TRPM8 Inhibition Regulates the Proliferation, Migration and ROS Metabolism of Bladder Cancer Cells.OncoTargets and therapy · 2020Article
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several studies have shown that transient receptor potential cation channel subfamily M member 8 (TRPM8), which has been regarded as a novel prostate-specific marker, serves a key role in processes such as the proliferation, viability and cell migration of prostate cancer cells. Efforts have been made to uncover the potential role of targeting TRPM8 in the management of prostate cancer; it has been verified that TRPM8-targeted blockade, either by RNA interference-mediated depletion or specific TRPM8 inhibitors, could reduce the rate of proliferation and proliferative fraction, and induce apoptosis in prostate cancer cells. The aim of the present study was to investigate the effect of knockdown of TRPM8 on chemosensitivity in prostate cancer LNCaP and PC3 cells. The RNA interference-mediated depletion of TRPM8 inhibited proliferation and enhanced epirubicin chemosensitivity of LNCaP and PC3 cells, and promoted epirubicin-induced apoptosis by increasing the phosphorylation of p38 mitogen-activated protein kinase (hereafter p38) and c-Jun N-terminal kinase (JNK)/mitogen-activated protein kinase signaling pathways, which was demonstrated via the use of specific inhibitors of phosphorylation of p38 and JNK. The results demonstrate that the targeted silencing of TRPM8 expression is a therapeutic strategy for treatment of prostate cancer that has considerable potential, even for castration-resistant prostate cancer.
Indexed as
Identifiers
What OpenQuestion holds
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.