Evidence map›Paper›PMID 28485104›Full record

ArticleThe Prostate2017

MicroRNA-181a promotes docetaxel resistance in prostate cancer cells.

Cameron M Armstrong, Chengfei Liu, Wei Lou, Alan P Lombard, Christopher P Evans, Allen C Gao

Abstract read
In one paragraph

Article in The Prostate, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 2 pooled it
1.5field-weighted citation impact, top 20% 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

20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  4. Review
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  7. Article
  8. Article
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  10. Article
  11. Review
  12. New Insights into Mechanisms of Endocrine-Disrupting Chemicals in Thyroid Diseases: The Epigenetic Way.International journal of environmental research and public health · 2020
    Review
  13. Resistance Mechanisms to Taxanes and PARP Inhibitors in Advanced Prostate Cancer.Current opinion in endocrine and metabolic research · 2020
    Article
  14. Review
  15. Human antigen R and drug resistance in tumors.Investigational new drugs · 2019
    Review
  16. Article
  17. Expression of miR-195 and MEK1 in patients with bladder cancer and their relationship to prognosis.International journal of clinical and experimental pathology · 2019
    Article
  18. Article
  19. Review
  20. Article
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

6 authors at 3 institutions in 1 country.

Cameron M ArmstrongDepartment of Urology, University of California Davis, Sacramento, California.
Chengfei LiuDepartment of Urology, University of California Davis, Sacramento, California.
Wei LouDepartment of Urology, University of California Davis, Sacramento, California.
Alan P LombardDepartment of Urology, University of California Davis, Sacramento, California.
Christopher P EvansDepartment of Urology, University of California Davis, Sacramento, California.
Allen C GaoDepartment of Urology, University of California Davis, Sacramento, California.ORCID http://orcid.org/0000-0002-5966-9038
University of California, Davis · USUniversity of California Davis Medical Center · USVA Northern California Health Care System · US

Funding

Novel roles of microRNA in androgen receptor signalingR01CA168601 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI GAO, ALLEN C. · 2013 to 2017
$1.5M
Interleukin-6 and castration-resistant prostate cancerR01CA140468 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI GAO, ALLEN C. · 2010 to 2014
$1.5M
(PQD-1) NF-kB activation and enzalutamide therapy in metastatic castration resistR21CA179970 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI GAO, ALLEN C. · 2013 to 2014
$363k
The role of p52 in prostate cancerI01BX002653 · VA · VA NORTHERN CALIFORNIA HEALTH CARE SYS · PI GAO, ALLEN C. · 2014 to 2017
–
BLRD VA I01 BX002653NCI NIH HHS R01 CA140468NCI NIH HHS R01 CA168601NCI NIH HHS R21 CA179970
6 · The paper itself

Abstract

backgroundDocetaxel is one of the primary drugs used for treating castration resistant prostate cancer (CRPC). Unfortunately, over time patients invariably develop resistance to docetaxel therapy and their disease will continue to progress. The mechanisms by which resistance develops are still incompletely understood. This study seeks to determine the involvement of miRNAs, specifically miR-181a, in docetaxel resistance in CRPC.

methodsReal-time PCR was used to measure miR-181a expression in parental and docetaxel resistant C4-2B and DU145 cells (TaxR and DU145-DTXR). miR-181a expression was modulated in parental or docetaxel resistant cells by transfecting them with miR-181a mimics or antisense, respectively. Following transfection, cell number was determined after 48 h with or without docetaxel. Cross resistance to cabazitaxel induced by miR-181a was also determined. Western blots were used to determine ABCB1 protein expression and rhodamine assays used to assess activity. Phospho-p53 expression was assessed by Western blot and apoptosis was measured by ELISA in C4-2B TaxR and PC3 cells with inhibited or overexpressed miR-181a expression with or without docetaxel.

resultsmiR-181a is significantly overexpressed in TaxR and DU145-DTXR cells compared to parental cells. Overexpression of miR-181a in parental cells confers docetaxel and cabazitaxel resistance and knockdown of miR-181a in TaxR cells re-sensitizes them to treatment with both docetaxel and cabazitaxel. miR-181a was not observed to impact ABCB1 expression or activity, a protein which was previously demonstrated to be highly involved in docetaxel resistance. Knockdown of miR-181a in TaxR cells induced phospho-p53 expression. Furthermore, miR-181a knockdown alone induced apoptosis in TaxR cells which could be further enhanced by the addition of DTX.

conclusionsOverexpression of mir-181a in prostate cancer cells contributes to their resistance to docetaxel and cabazitaxel and inhibition of mir-181a expression can restore treatment response. This is due, in part, to modulation of p53 phosphorylation and apoptosis.

Indexed as

ProstateProstatic Neoplasms, Castration-ResistantTaxoidsAntineoplastic AgentsCell Line, TumorDocetaxelDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansMaleMicroRNAsPharmacogeneticsAntineoplastic AgentscabazitaxelDocetaxelMicroRNAsMIrn181 microRNA, humanTaxoidsdocetaxelmiR-181aprostate cancerresistance

Identifiers

PMID28485104
PMCPMC5448975
OpenAlexW2612955121

What OpenQuestion holds

Textmetadata
LicenceTDM
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.