Evidence map›Paper›PMID 28039451›Full record

ArticleOncotarget2017

High-throughput proteome analysis reveals targeted TRPM8 degradation in prostate cancer.

Swapna Asuthkar, Lusine Demirkhanyan, Samuel Robert Mueting, Alejandro Cohen, Eleonora Zakharian

Abstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. TRPM8 as the rapid testosterone signaling receptor: Implications in the regulation of dimorphic sexual and social behaviors.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  8. The Presence and Distribution of TRPM7 in the Canine Mammary Glands.Animals : an open access journal from MDPI · 2020
    Article
  9. Article
  10. Article
  11. TRPM8 and prostate: a cold case?Pflugers Archiv : European journal of physiology · 2018
    Review
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

5 authors.

Swapna AsuthkarUniversity of Illinois College of Medicine, Department of Cancer Biology and Pharmacology, Peoria, IL 61605, USA.
Lusine DemirkhanyanUniversity of Illinois College of Medicine, Department of Cancer Biology and Pharmacology, Peoria, IL 61605, USA.
Samuel Robert MuetingUniversity of Illinois College of Medicine, Department of Cancer Biology and Pharmacology, Peoria, IL 61605, USA.
Alejandro CohenProteomics and Mass Spectrometry Core Facility, Life Sciences Research Institute, Dalhousie University, Halifax, NS B3H 4R2, Canada.
Eleonora ZakharianUniversity of Illinois College of Medicine, Department of Cancer Biology and Pharmacology, Peoria, IL 61605, USA.

Funding

TRP channels in supramolecular complexes with Inorganic Polyphosphate and PolyhydR01GM098052 · NIGMS · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI ZAKHARIAN, ELEONORA · 2011 to 2015
$1.5M
NIGMS NIH HHS R01 GM098052
6 · The paper itself

Abstract

The Ca2+-permeable ion channel TRPM8 is a hallmark of the prostate epithelium. We recently discovered that TRPM8 is an ionotropic testosterone receptor. This finding suggested that testosterone-induced TRPM8 activity regulates Ca2+ homeostasis in the prostate epithelium. Since androgens are significantly implicated in prostate cancer development, the role of the novel testosterone receptor TRPM8 in cancer was assessed in our study. Although TRPM8 mRNA levels increase at the early prostate cancer stages, we found that it is not proportionally translated into TRPM8 protein levels. High-throughput proteome analysis revealed that TRPM8 degradation is enhanced in human prostate cancer cells. This degradation is executed via a dual degradation mechanism with the involvement of both lysosomal and proteasomal proteolytic pathways. The evaluation of the TRPM8 expression pattern in prostate cancer patients further confirmed the incidence of TRPM8 removal from the plasma membrane and its internalization pattern coincided with the severity of the tumor. Together, our results indicate that enhanced TRPM8 hydrolysis in prostate cancer could present an adaptation mechanism, sustained via bypassing testosterone-induced rapid Ca2+ uptake through TRPM8, thus, diminishing the rates of apoptosis. In this light, recovery of TRPM8 may pose a novel therapeutic strategy for an anti-tumor defense mechanism.

Indexed as

Cell Line, TumorHigh-Throughput Screening AssaysHumansImmunoblottingImmunohistochemistryImmunoprecipitationMaleMass SpectrometryProstatic NeoplasmsProteomeProteomicsTRPM Cation ChannelsProteomeTRPM8 protein, humanTRPM Cation Channelsandrogensprostate cancerprotein degradationtestosteronetransient receptor potential melastatin 8 channel (TRPM8)

Identifiers

PMID28039451
PMCPMC5355063

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Registered trials

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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 OpenQuestion graph.