Evidence map›Paper›PMID 21927026›Full record

ArticleOncogene2012

Self-renewal gene tracking to identify tumour-initiating cells associated with metastatic potential.

C Y Darini, D F Pisani, P Hofman, F Pedeutour, I Sudaka, C Chomienne, C Dani, A Ladoux

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Multifaceted role ofiScience · 2026
    Article
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  3. Article
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  8. Article
  9. Article
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  11. Review
  12. The Oct4 protein: more than a magic stemness marker.American journal of stem cells · 2014
    Review
  13. Article
  14. 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.

C Y DariniCNRS, Institute of Biology Development and Cancer, University of Nice Sophia-Antipolis, 28 Avenue de Valombrose, Nice Cedex 2, France.
D F Pisani
P Hofman
F Pedeutour
I Sudaka
C Chomienne
C Dani
A Ladoux

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumour-initiating cells (TICs) are rare cancer cells isolated from tumours of different origins including high-grade tumours that sustain neoplasic progression and development of metastatic disease. They harbour deregulated stem cells pathways and exhibit an unchecked ability to self-renew, a property essential for tumour progression. Among the essential factors maintaining embryonic stem (ES) cells properties, OCT-4 (also known as POU5F1) has been detected in tumours of different origins. Although ectopic expression results in dysplasic growth restricted to epithelial tissues, overexpression expands the proportion of immature cells in teratomas. However, OCT-4-expressing cells have not been purified from spontaneously occurring tumours, thus information concerning their properties is rather scant. Here, using p53-/- mice expressing green fluorescent protein and the puromycin resistance gene under the control of the Oct-4 promoter, we show that OCT-4 is expressed in 5% onwards of the undifferentiated tumour cell populations derived from different organs. OCT-4 expression was low as compared with ES cells, but was associated with a 'stemness' signature and expression of the chemokine receptor CXCR4. These cells displayed cancer stem cell features, including increased self-renewal and differentiation ability in vitro and in vivo. They not only formed allografts containing immature bone regions but also disseminated into different organs, including lung, liver and bone. Experiments based on RNA interference revealed that Oct-4 expression drives both their engraftment and metastasis formation. This work points out the crucial contribution of Oct-4-expressing TICs in the hierarchical organization of the malignant potential, leading to metastasis formation. Consequently, it provides an appropriate model to develop novel therapies aiming to strike down TICs by targeting self-renewal genes, therefore efficient to reduce tumour growth and metastatic disease.

Indexed as

AnimalsBiomarkers, TumorCell Transformation, NeoplasticDisease Models, AnimalEmbryonic Stem CellsGene Expression ProfilingGene Expression Regulation, NeoplasticMiceMice, SCIDNeoplasm MetastasisNeoplasm TransplantationNeoplastic Stem CellsOctamer Transcription Factor-3Promoter Regions, GeneticPuromycinReceptors, CXCR4Biomarkers, TumorCXCR4 protein, mouseOctamer Transcription Factor-3Pou5f1 protein, mousePuromycinReceptors, CXCR4RNA, Small InterferingTumor Suppressor Protein p53

Identifiers

PMID21927026

What OpenQuestion holds

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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.