Evidence map›Paper›PMID 20805998›Full record

ArticlePloS one2010

Epithelial to mesenchymal transition is mechanistically linked with stem cell signatures in prostate cancer cells.

Dejuan Kong, Sanjeev Banerjee, Aamir Ahmad, Yiwei Li, Zhiwei Wang, Seema Sethi, Fazlul H Sarkar

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 230 papers.

0numbers the graph read from it
0cells of the map it votes in
230citing papers in PubMed
23.8field-weighted citation impact, top 1% 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

230 citing papers in PubMed, 403 citations in OpenAlex.

  1. Trial
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  6. Implications of Heterotypic Cell Fusion in Cancer.Advances in experimental medicine and biology · 2026
    Review
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  12. Article
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  19. Review
  20. Impact of cell plasticity on prostate tumor heterogeneity and therapeutic response.American journal of clinical and experimental urology · 2024
    Review

170 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

7 authors at 2 institutions in 1 country.

Dejuan KongDepartment of Pathology, Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, Michigan, United States of America.
Sanjeev Banerjee
Aamir Ahmad
Yiwei Li
Zhiwei Wang
Seema Sethi
Fazlul H Sarkar
Wayne State University · USThe Barbara Ann Karmanos Cancer Institute · US

Funding

Molecular Mechanism of Genistein (Isoflavone) in Prostate CancerR01CA083695 · NCI · WAYNE STATE UNIVERSITY · PI SARKAR, FAZLUL H. · 2001 to 2011
$2.3M
Mechanistic Role of miRNAs and Their Targets in Prostate Cancer AggressivenessR01CA164318 · NCI · WAYNE STATE UNIVERSITY · PI SARKAR, FAZLUL H. · 2012 to 2015
$1.3M
NCI NIH HHS 5R01CA083695-08NCI NIH HHS R01 CA083695NCI NIH HHS R01 CA164318
6 · The paper itself

Abstract

backgroundCurrent management of patients diagnosed with prostate cancer (PCa) is very effective; however, tumor recurrence with Castrate Resistant Prostate Cancer (CRPC) and subsequent metastasis lead to poor survival outcome, suggesting that there is a dire need for novel mechanistic understanding of tumor recurrence, which would be critical for designing novel therapies. The recurrence and the metastasis of PCa are tightly linked with the biology of prostate cancer stem cells or cancer-initiating cells that is reminiscent of the acquisition of Epithelial to Mesenchymal Transition (EMT) phenotype. Increasing evidence suggests that EMT-type cells share many biological characteristics with cancer stem-like cells. METHODOLOGY/PRINCIPAL

findingsIn this study, we found that PCa cells with EMT phenotype displayed stem-like cell features characterized by increased expression of Sox2, Nanog, Oct4, Lin28B and/or Notch1, consistent with enhanced clonogenic and sphere (prostasphere)-forming ability and tumorigenecity in mice, which was associated with decreased expression of miR-200 and/or let-7 family. Reversal of EMT by re-expression of miR-200 inhibited prostasphere-forming ability of EMT-type cells and reduced the expression of Notch1 and Lin28B. Down-regulation of Lin28B increased let-7 expression, which was consistent with repressed self-renewal capability. CONCLUSIONS/SIGNIFICANCE: These results suggest that miR-200 played a pivotal role in linking the characteristics of cancer stem-like cells with EMT-like cell signatures in PCa. Selective elimination of cancer stem-like cells by reversing the EMT phenotype to Mesenchymal-Epithelial Transition (MET) phenotype using novel agents would be useful for the prevention of tumor recurrence especially by eliminating those cells that are the "Root Cause" of tumor development and recurrence.

Indexed as

AnimalsBase SequenceBiomarkersCell DifferentiationCell Line, TumorDNA-Binding ProteinsDown-RegulationEpithelial CellsGene Expression ProfilingHomeodomain ProteinsHumansLymphokinesMaleMesodermMiceMicroRNAsBiomarkersDNA-Binding ProteinsHomeodomain ProteinsLIN28B protein, humanLymphokinesMicroRNAsMIRN200 microRNA, humanmirnlet7 microRNA, humanNanog Homeobox ProteinNANOG protein, humanOctamer Transcription Factor-3PDGFD protein, humanPlatelet-Derived Growth FactorPOU5F1 protein, humanReceptor, Notch1RNA-Binding ProteinsSOX2 protein, humanSOXB1 Transcription Factors

Identifiers

PMID20805998
PMCPMC2929211
OpenAlexW1971707325

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.