Evidence map›Paper›PMID 28642484›Full record

ArticleScientific reports2017

miR-100-5p inhibition induces apoptosis in dormant prostate cancer cells and prevents the emergence of castration-resistant prostate cancer.

Noushin Nabavi, Nur Ridzwan Nur Saidy, Erik Venalainen, Anne Haegert, Abhijit Parolia, Hui Xue, Yuwei Wang, Rebecca Wu, Xin Dong, Colin Collins and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

27 citing papers in PubMed, 48 citations in OpenAlex.

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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

12 authors at 3 institutions in 1 country.

Noushin NabaviExperimental Therapeutics, BC Cancer Research Centre, Vancouver, BC, Canada.
Nur Ridzwan Nur SaidyHonors Biotechnology Program, Department of Microbiology and Immunology, University of British Columbia, 2329 West Mall, Vancouver, BC, V6T 1Z4, Canada.
Erik VenalainenHonors Biotechnology Program, Department of Microbiology and Immunology, University of British Columbia, 2329 West Mall, Vancouver, BC, V6T 1Z4, Canada.
Anne HaegertThe Vancouver Prostate Centre, Vancouver General Hospital, Vancouver, BC, Canada.
Abhijit ParoliaHonors Biotechnology Program, Department of Microbiology and Immunology, University of British Columbia, 2329 West Mall, Vancouver, BC, V6T 1Z4, Canada.
Hui XueExperimental Therapeutics, BC Cancer Research Centre, Vancouver, BC, Canada.
Yuwei WangExperimental Therapeutics, BC Cancer Research Centre, Vancouver, BC, Canada.
Rebecca WuExperimental Therapeutics, BC Cancer Research Centre, Vancouver, BC, Canada.
Xin DongExperimental Therapeutics, BC Cancer Research Centre, Vancouver, BC, Canada.
Colin CollinsThe Vancouver Prostate Centre, Vancouver General Hospital, Vancouver, BC, Canada.
Francesco CreaExperimental Therapeutics, BC Cancer Research Centre, Vancouver, BC, Canada. francesco.crea@open.ac.uk.
Yuzhuo WangExperimental Therapeutics, BC Cancer Research Centre, Vancouver, BC, Canada. ywang@bccrc.ca.
BC Cancer Agency · CAVancouver General Hospital · CAUniversity of British Columbia · CA

Funding

Cancer Research UK 22592
6 · The paper itself

Abstract

Carcinoma of the prostate is the most common cancer in men. Treatment of aggressive prostate cancer involves a regiment of radical prostectomy, radiation therapy, chemotherapy and hormonal therapy. Despite significant improvements in the last decade, the treatment of prostate cancer remains unsatisfactory, because a significant fraction of prostate cancers develop resistance to multiple treatments and become incurable. This prompts an urgent need to investigate the molecular mechanisms underlying the evolution of therapy-induced resistance of prostate cancer either in the form of castration-resistant prostate cancer (CRPC) or transdifferentiated neuroendocrine prostate cancer (NEPC). By analyzing micro-RNA expression profiles in a set of patient-derived prostate cancer xenograft tumor lines, we identified miR-100-5p as one of the key molecular components in the initiation and evolution of androgen ablation therapy resistance in prostate cancer. In vitro results showed that miR-100-5p is required for hormone-independent survival and proliferation of prostate cancer cells post androgen ablation. In Silico target predictions revealed that miR-100-5p target genes are involved in key aspects of cancer progression, and are associated with clinical outcome. Our results suggest that mir-100-5p is a possible therapeutic target involved in prostate cancer progression and relapse post androgen ablation therapy.

Indexed as

AndrogensAnimalsApoptosisCell CycleCell Line, TumorCell ProliferationDisease Models, AnimalDisease ProgressionGene Expression ProfilingHumansMaleMiceMicroRNAsProstatic Neoplasms, Castration-ResistantRNA InterferenceSignal TransductionAndrogensMicroRNAsMIRN100 microRNA, human

Identifiers

PMID28642484
PMCPMC5481412
OpenAlexW2625285070

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.