Evidence map›Paper›PMID 24931166›Full record

ArticleOncogene2015

Antisense transcription at the TRPM2 locus as a novel prognostic marker and therapeutic target in prostate cancer.

U Orfanelli, E Jachetti, F Chiacchiera, M Grioni, P Brambilla, A Briganti, M Freschi, F Martinelli-Boneschi, C Doglioni, F Montorsi and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing 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

46 citing papers in PubMed.

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  15. A novel strategy for treating cancer: understanding the role of CaExploration of targeted anti-tumor therapy · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors.

U OrfanelliSan Raffaele Scientific Institute, Vita-Salute San Raffaele University and Center for Translational Genomics and Bioinformatics, Milan, Italy.
E JachettiSan Raffaele Scientific Institute, Cellular Immunology Unit, Milan, Italy.
F ChiacchieraDepartment of Experimental Oncology, European Institute of Oncology (IEO), Milan, Italy.
M GrioniSan Raffaele Scientific Institute, Cellular Immunology Unit, Milan, Italy.
P BrambillaSan Raffaele Scientific Institute, Division of Neuroscience, Institute of Experimental Neurology (INSPE), Laboratory of Genetics of Neurological Complex Disorders, Milan, Italy.
A BrigantiSan Raffaele Scientific Institute, Vita-Salute San Raffaele University and Department of Urology, Milan, Italy.
M FreschiDepartment of Pathology, Vita-Salute University San Raffaele, Milan, Italy.
F Martinelli-BoneschiSan Raffaele Scientific Institute, Division of Neuroscience, Institute of Experimental Neurology (INSPE), Laboratory of Genetics of Neurological Complex Disorders, Milan, Italy.
C DoglioniDepartment of Pathology, Vita-Salute University San Raffaele, Milan, Italy.
F MontorsiSan Raffaele Scientific Institute, Vita-Salute San Raffaele University and Department of Urology, Milan, Italy.
M BelloneSan Raffaele Scientific Institute, Cellular Immunology Unit, Milan, Italy.
G CasariSan Raffaele Scientific Institute, Vita-Salute San Raffaele University and Center for Translational Genomics and Bioinformatics, Milan, Italy.
D PasiniDepartment of Experimental Oncology, European Institute of Oncology (IEO), Milan, Italy.
G LavorgnaSan Raffaele Scientific Institute, Vita-Salute San Raffaele University and Center for Translational Genomics and Bioinformatics, Milan, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Overwhelming evidence indicates that cancer is a genetic disease caused by the accumulation of mutations in oncogenes and tumor suppressor genes. It is also increasingly apparent, however, that cancer depends not only on mutations in these coding genes but also on alterations in the large class of non-coding RNAs. Here, we report that one such long non-coding RNA, TRPM2-AS, an antisense transcript of TRPM2, which encodes an oxidative stress-activated ion channel, is overexpressed in prostate cancer (PCa). The high expression of TRPM2-AS and its related gene signature were found to be linked to poor clinical outcome, with the related gene signature working also independently of the patient's Gleason score. Mechanistically, TRPM2-AS knockdown led to PCa cell apoptosis, with a transcriptional profile that indicated an unbearable increase in cellular stress in the dying cells, which was coupled to cell cycle arrest, an increase in intracellular hydrogen peroxide and activation of the sense TRPM2 gene. Moreover, targets of existing drugs and treatments were found to be consistently associated with high TRPM2-AS levels in both targeted cells and patients, ultimately suggesting that the measurement of the expression levels of TRPM2-AS allows not only for the early identification of aggressive PCa tumors, but also identifies a subset of at-risk patients who would benefit from currently available, but mostly differently purposed, therapeutic agents.

Indexed as

ApoptosisBiomarkers, TumorCell Cycle CheckpointsCell Line, TumorEndoplasmic Reticulum StressHumansHydrogen PeroxideMaleOxidative StressPrognosisProstatic NeoplasmsRNA, AntisenseRNA InterferenceRNA, Small InterferingTranscription, GeneticTRPM Cation ChannelsBiomarkers, TumorHydrogen PeroxideRNA, AntisenseRNA, Small InterferingTRPM2 protein, humanTRPM Cation Channels

Identifiers

PMID24931166

What OpenQuestion holds

Textmetadata
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.