Evidence map›Paper›PMID 26496025›Full record

ArticleOncotarget2015

Transient receptor potential melastatin 4 channel contributes to migration of androgen-insensitive prostate cancer cells.

Christian Holzmann, Sven Kappel, Tatiana Kilch, Marcus Martin Jochum, Sabine Katharina Urban, Volker Jung, Michael Stöckle, Karen Rother, Markus Greiner, Christine Peinelt

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 15% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

  1. Pooled it
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  6. The Role of TRPM7 in Oncogenesis.International journal of molecular sciences · 2024
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  9. Monitoring trafficking and expression of hemagglutinin-tagged transient receptor potential melastatin 4 channel in mammalian cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Christian HolzmannBiophysics, Center for Integrative Physiology and Molecular Medicine, School of Medicine, Saarland University, Homburg, Germany.
Sven KappelBiophysics, Center for Integrative Physiology and Molecular Medicine, School of Medicine, Saarland University, Homburg, Germany.
Tatiana KilchBiophysics, Center for Integrative Physiology and Molecular Medicine, School of Medicine, Saarland University, Homburg, Germany.
Marcus Martin JochumCenter of Human and Molecular Biology, Saarland University, Homburg, Germany.
Sabine Katharina UrbanCenter of Human and Molecular Biology, Saarland University, Homburg, Germany.
Volker JungClinics of Urology and Pediatric Urology, Saarland University, Homburg, Germany.
Michael StöckleClinics of Urology and Pediatric Urology, Saarland University, Homburg, Germany.
Karen RotherCenter of Human and Molecular Biology, Saarland University, Homburg, Germany.
Markus GreinerCenter of Human and Molecular Biology, Saarland University, Homburg, Germany.
Christine PeineltBiophysics, Center for Integrative Physiology and Molecular Medicine, School of Medicine, Saarland University, Homburg, Germany.
Saarland University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Impaired Ca2+ signaling in prostate cancer contributes to several cancer hallmarks, such as enhanced proliferation and migration and a decreased ability to induce apoptosis. Na+ influx via transient receptor potential melastatin 4 channel (TRPM4) can reduce store-operated Ca2+ entry (SOCE) by decreasing the driving force for Ca2+. In patients with prostate cancer, gene expression of TRPM4 is elevated. Recently, TRPM4 was identified as a cancer driver gene in androgen-insensitive prostate cancer.We investigated TRPM4 protein expression in cancer tissue samples from 20 patients with prostate cancer. We found elevated TRPM4 protein levels in prostatic intraepithelial neoplasia (PIN) and prostate cancer tissue compared to healthy tissue. In primary human prostate epithelial cells (hPEC) from healthy tissue and in the androgen-insensitive prostate cancer cell lines DU145 and PC3, TRPM4 mediated large Na+ currents. We demonstrated significantly increased SOCE after siRNA targeting of TRPM4 in hPEC and DU145 cells. In addition, knockdown of TRPM4 reduced migration but not proliferation of DU145 and PC3 cells. Taken together, our data identify TRPM4 as a regulator of SOCE in hPEC and DU145 cells, demonstrate a role for TRPM4 in cancer cell migration and suggest that TRPM4 is a promising potential therapeutic target.

Indexed as

Cell MovementCalcium SignalingCell Line, TumorGene Expression Regulation, NeoplasticHumansMaleMembrane PotentialsNeoplasm InvasivenessProstatic Intraepithelial NeoplasiaProstatic NeoplasmsProstatic Neoplasms, Castration-ResistantRNA InterferenceSodiumTime FactorsTransfectionTRPM Cation ChannelsSodiumTRPM4 protein, humanTRPM Cation ChannelsCa2+ signalingcancer driver genecell migrationprostate cancertransient receptor potential melastatin 4 channel (TRPM4)

Identifiers

PMID26496025
PMCPMC4747188
OpenAlexW2253189753

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.