Evidence map›Paper›PMID 25228591›Full record

ArticleOncotarget2014

Induced cancer stem-like cells as a model for biological screening and discovery of agents targeting phenotypic traits of cancer stem cell.

Mayuko Nishi, Hidenori Akutsu, Ayumi Kudoh, Hirokazu Kimura, Naoki Yamamoto, Akihiro Umezawa, Sam W Lee, Akihide Ryo

Abstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

  1. FUT2-Mediated Fucosylation of OLFM4 Promotes Colon Cancer Cell Differentiation.Canadian journal of gastroenterology & hepatology · 2026
    Article
  2. Article
  3. Advances in ovarian tumor stem cells and therapy.Cell biochemistry and biophysics · 2024
    Review
  4. Review
  5. Article
  6. Article
  7. Calcium Channels as Novel Therapeutic Targets for Ovarian Cancer Stem Cells.International journal of molecular sciences · 2020
    Article
  8. Potential application of cell reprogramming techniques for cancer research.Cellular and molecular life sciences : CMLS · 2019
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
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  19. 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

8 authors.

Mayuko NishiDepartment of Microbiology, Yokohama City University School of Medicine, Yokohama, Japan.
Hidenori AkutsuDepartment of Reproductive Biology, National Research Institute for Child Health and Development, Tokyo, Japan.
Ayumi KudohDepartment of Microbiology, Yokohama City University School of Medicine, Yokohama, Japan.
Hirokazu KimuraInfectious Disease Surveillance Center, National Institute of Infectious Diseases, Tokyo, Japan.
Naoki YamamotoDepartment of Microbiology, National University of Singapore, Singapore.
Akihiro UmezawaDepartment of Reproductive Biology, National Research Institute for Child Health and Development, Tokyo, Japan.
Sam W LeeCutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Akihide RyoDepartment of Microbiology, Yokohama City University School of Medicine, Yokohama, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer stem cells (CSCs) retain the capacity to propagate themselves through self-renewal and to produce heterogeneous lineages of cancer cells constituting the tumor. Novel drugs that target CSCs can potentially eliminate the tumor initiating cell population therefore resulting in complete cure of the cancer. We recently established a CSC-like model using induced pluripotent stem cell (iPSC) technology to reprogram and partially differentiate human mammary epithelial MCF-10A cells. Using the induced CSC-like (iCSCL) model, we developed a phenotypic drug assay system to identify agents that inhibit the stemness and self-renewal properties of CSCs. The selectivity of the agents was assessed using three distinct assays characterized by cell viability, cellular stemness and tumor sphere formation. Using this approach, we found that withaferin A (WA), an Ayurvedic medicine constituent, was a potent inhibitor of CSC stemness leading to cellular senescence primarily via the induction of p21Cip1 expression. Moreover, WA exhibited strong anti-tumorigenic activity against the iCSCL. These results indicate that our iCSCL model provides an innovative high throughput platform for a simple, easy, and cost-effective method to search for novel CSC-targeting drugs. Furthermore, our current study identified WA as a putative drug candidate for abrogating the stemness and tumor initiating ability of CSCs.

Indexed as

High-Throughput Screening AssaysAnimalsAntineoplastic AgentsCell DifferentiationCell LineCell LineageCell MovementCell ProliferationCell SurvivalCell Transformation, NeoplasticCellular ReprogrammingCellular SenescenceCyclin-Dependent Kinase Inhibitor p21Dose-Response Relationship, DrugDrug DiscoveryEpithelial-Mesenchymal TransitionAntineoplastic AgentsCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21withaferin AWithanolides

Identifiers

PMID25228591
PMCPMC4226712

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.