Evidence map›Paper›PMID 20224986›Full record

ArticleMolecular and cellular biochemistry2010

Establishment and characterization of multi-drug resistant, prostate carcinoma-initiating stem-like cells from human prostate cancer cell lines 22RV1.

Te Liu, Fuhui Xu, Xiling Du, Dongmei Lai, Tianjin Liu, Yarui Zhao, Qin Huang, Lizhen Jiang, Wenbin Huang, Weiwei Cheng and 1 more

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing 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

69 citing papers in PubMed.

  1. Article
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  5. Review
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  9. Glutathione S-Transferases in Cancer.Antioxidants (Basel, Switzerland) · 2021
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Epigenetic Silencing of miRNA-338-5p and miRNA-421 Drives SPINK1-Positive Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Article
  20. Article

9 more citing papers are in PubMed but not listed here.

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

11 authors.

Te LiuSchool of Life Science and Technology, Tongji University, 200092 Shanghai, China.
Fuhui Xu
Xiling Du
Dongmei Lai
Tianjin Liu
Yarui Zhao
Qin Huang
Lizhen Jiang
Wenbin Huang
Weiwei Cheng
Zhixue Liu

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multi-drug resistance is an important element which leads to ineffectiveness of chemotherapeutics. To identify subpopulations of cancerous prostate cells with multi-drug resistance and cancer stem-cell properties has recently become a major research interest. We identified a subpopulation from the prostate cancer cell line 22RV1, which have high surface expression of both CD117 and ABCG2. We found this subpopulation of cells termed CD117(+)/ABCG2(+) also overexpress stem cells markers such as Nanog, Oct4, Sox2, Nestin, and CD133. These cells are highly prolific and are also resistant to treatment with a variety of chemotherapeutics such as casplatin, paclitaxel, adriamycin, and methotrexate. In addition, CD117(+)/ABCG2(+) cells can readily establish tumors in vivo in a relatively short time. To investigate the mechanism of aggressive tumor growth and drug resistance, we examined the CpG islands on the ABCG2 promoter of CD117(+)/ABCG2(+) cells and found they were remarkably hypomethylated. Furthermore, chromatin immunoprecipitation assays revealed high levels of both histone 3 acetylation and H3K4 trimethylation at the CpG islands on the ABCG2 promoter. Our these data suggest that CD117(+)/ABCG2(+) cells could be reliably sorted from the human prostate cancer cell line 22RV1, and represent a valuable model for studying cancer cell physiology and multi-drug resistance. Furthermore, identification and study of these cells could have a profound impact on selection of individual treatment strategies, clinical outcome, and the design or selection of the next generation of chemotherapeutic agents.

Indexed as

Drug Resistance, NeoplasmAcetylationAnimalsAntineoplastic AgentsATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 2AzacitidineBiomarkers, TumorCell Line, TumorCell ProliferationCpG IslandsDecitabineDNA MethylationDNA Modification MethylasesEnzyme InhibitorsEpigenesis, GeneticABCG2 protein, humanAntineoplastic AgentsATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 2AzacitidineBiomarkers, TumorDecitabineDNA Modification MethylasesEnzyme InhibitorsHistonesNeoplasm ProteinsProto-Oncogene Proteins c-kit

Identifiers

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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.