Evidence map›Paper›PMID 26110651›Full record

ArticlePloS one2015

Enrichment of the Cancer Stem Phenotype in Sphere Cultures of Prostate Cancer Cell Lines Occurs through Activation of Developmental Pathways Mediated by the Transcriptional Regulator ΔNp63α.

Roberto Portillo-Lara, Mario Moisés Alvarez

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. 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
1.1field-weighted citation impact, top 21% 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, 38 citations in OpenAlex.

  1. Article
  2. The dual role of p63 in cancer.Frontiers in oncology · 2023
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Stem cells from a malignant rat prostate cell line generate prostate cancersAmerican journal of clinical and experimental urology · 2022
    Article
  9. Article
  10. Article
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  13. NANOG helps cancer cells escape NK cell attack by downregulating ICAM1 during tumorigenesis.Journal of experimental & clinical cancer research : CR · 2019
    Article
  14. Review
  15. Article
  16. Article
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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

2 authors at 2 institutions in 2 countries.

Roberto Portillo-LaraCentro de Biotecnología-FEMSA, Tecnológico de Monterrey, Monterrey, Nuevo León, México.
Mario Moisés AlvarezCentro de Biotecnología-FEMSA, Tecnológico de Monterrey, Monterrey, Nuevo León, México; Harvard-MIT Health Sciences and Technology, Brigham and Women's Hospital, Cambridge, Massachusetts, United States of America.
Brigham and Women's Hospital · USTecnológico de Monterrey · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCancer stem cells (CSC) drive prostate cancer tumor survival and metastasis. Nevertheless, the development of specific therapies against CSCs is hindered by the scarcity of these cells in prostate tissues. Suspension culture systems have been reported to enrich CSCs in primary cultures and cell lines. However, the molecular mechanisms underlying this phenomenon have not been fully explored. METHODOLOGY/PRINCIPAL

findingsWe describe a prostasphere assay for the enrichment of CD133+ CSCs in four commercial PCa cell lines: 22Rv1, DU145, LNCaP, and PC3. Overexpression of CD133, as determined by flow cytometric analysis, correlated with an increased clonogenic, chemoresistant, and invasive potential in vitro. This phenotype is concordant to that of CSCs in vivo. Gene expression profiling was then carried out using the Cancer Reference panel and the nCounter system from NanoString Technologies. This analysis revealed several upregulated transcripts that can be further explored as potential diagnostic markers or therapeutic targets. Furthermore, functional annotation analysis suggests that ΔNp63α modulates the activation of developmental pathways responsible for the increased stem identity of cells growing in suspension cultures. CONCLUSIONS/SIGNIFICANCE: We conclude that profiling the genetic mechanisms involved in CSC enrichment will help us to better understand the molecular pathways that underlie CSC pathophysiology. This platform can be readily adapted to enrich and assay actual patient samples, in order to design patient-specific therapies that are aimed particularly against CSCs.

Indexed as

AC133 AntigenAntigens, CDBiomarkers, TumorCell Line, TumorGene Expression ProfilingGene Expression Regulation, NeoplasticGlycoproteinsHumansMaleNeoplastic Stem CellsPeptidesPhenotypeProstatic NeoplasmsAC133 AntigenAntigens, CDBiomarkers, TumorGlycoproteinsPeptidesPROM1 protein, human

Identifiers

PMID26110651
PMCPMC4481544
OpenAlexW746610600

What OpenQuestion holds

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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.