Evidence map›Paper›PMID 30621625›Full record

ArticleBMC cancer2019

Targeting Ezh2 could overcome docetaxel resistance in prostate cancer cells.

Xiaofu Qiu, Wei Wang, Bijun Li, Bo Cheng, Kangjian Lin, Jian Bai, Huanhui Li, Guosheng Yang

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  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

8 authors at 5 institutions in 1 country.

Xiaofu QiuDepartment of Urology, Southern Medical University Third Medical College, Guangzhou, 510317, China. xfqiu123@163.com.
Wei WangDepartment of Urology, Guangzhou General Hospital of Guangzhou Military Command, Guangzhou, 510515, China.
Bijun LiDepartment of Urology, the Second Affiliated Hospital of Guangdong Medical College, Zhanjiang, 524003, China.
Bo ChengDepartment of Urology, the Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Kangjian LinDepartment of Urology, Southern Medical University Third Medical College, Guangzhou, 510317, China.
Jian BaiDepartment of Urology, Guangdong Second Provincial General Hospital, Guangzhou, 510317, China.
Huanhui LiDepartment of Urology, Guangdong Second Provincial General Hospital, Guangzhou, 510317, China.
Guosheng YangDepartment of Urology, Southern Medical University Third Medical College, Guangzhou, 510317, China. 2008yangguosheng@sina.com.
Third Affiliated Hospital of Southern Medical University · CNGuangdong Provincial People's Hospital · CNAffiliated Hospital of Southwest Medical University · CNGeneral Hospital of Guangzhou Military Command · CNGuangdong Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDocetaxel was used to treat metastatic CRPC patients. However, Doc resistance in prostate cancer (PCa) hinders its clinical application.

objectiveTo understand the underlying mechanisms by which Doc resistance is developed and to find novel therapeutic target to cure Doc resistant PCa has clinical importance.

methodsWe established Doc resistant cell lines and explored the role of Ezh2 in the development of Doc resistance by overexpressing its cDNA or using its inhibitor.

resultsWe found that Ezh2 was induced in our established Doc resistant (DocR) cells, which was attributable to the silenced expression of miR-101-3p and miR-138-5p. Blockage of Ezh2 activity by either inhibitor or miRNA mimics could overcome Doc resistance by suppressing Doc-induced cancer stem cells populations. Mechanistically, Ezh2 activity was required for the induced expression of Nanog, Sox2 and CD44 upon Doc treatment.

conclusionsTargeting Ezh2 could overcome Doc resistance.

Indexed as

ApoptosisCell Line, TumorCell ProliferationDocetaxelDrug Resistance, NeoplasmEnhancer of Zeste Homolog 2 ProteinGene Expression Regulation, NeoplasticHumansMaleMicroRNAsProstateProstatic NeoplasmsDocetaxelEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanMicroRNAsMIRN101 microRNA, humanMIRN138 microRNA, human

Identifiers

PMID30621625
PMCPMC6324167
OpenAlexW2917569933

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.