Evidence map›Paper›PMID 21102523›Full record

ArticleOncogene2011

Transforming growth factor-β regulates the sphere-initiating stem cell-like feature in breast cancer through miRNA-181 and ATM.

Y Wang, Y Yu, A Tsuyada, X Ren, X Wu, K Stubblefield, E K Rankin-Gee, S E Wang

Abstract read
In one paragraph

Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers.

0numbers the graph read from it
0cells of the map it votes in
154citing papers in PubMed
10.9field-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

154 citing papers in PubMed, 262 citations in OpenAlex.

  1. Trial
  2. Article
  3. CouldBiomedicines · 2025
    Article
  4. Review
  5. Non-Coding RNAs in Breast Cancer: Diagnostic and Therapeutic Implications.International journal of molecular sciences · 2024
    Review
  6. Expert opinion on therapeutic targets · 2024
    Review
  7. Review
  8. Review
  9. Advances in molecular targeted therapies to increase efficacy of (chemo)radiation therapy.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2023
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

94 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

8 authors at 4 institutions in 2 countries.

Y WangDivision of Tumor Cell Biology, Beckman Research Institute of City of Hope, Duarte, CA 91010, USA.
Y Yu
A Tsuyada
X Ren
X Wu
K Stubblefield
E K Rankin-Gee
S E Wang
Beckman Research InstituteCity Of Hope National Medical Center · USCity of Hope · USTianjin Medical University Cancer Institute and Hospital · CN

Funding

Crosstalk TGFbeta and HER2 (ErbB2) Signaling in Mammary TumorigenesisR00CA125892 · NCI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI WANG, SHIZHEN EMILY · 2009 to 2011
$906k
Crosstalk TGFbeta and HER2 (ErbB2) Signaling in Mammary TumorigenesisK99CA125892 · NCI · VANDERBILT UNIVERSITY · PI WANG, SHIZHEN EMILY · 2007 to 2008
$238k
NCI NIH HHS K99 CA125892NCI NIH HHS R00 CA125892
6 · The paper itself

Abstract

Recent studies indicate that a subset of cancer cells possessing stem cell properties, referred to as cancer-initiating or cancer stem cells (CSCs), have crucial roles in tumor initiation, metastasis and resistance to anticancer therapies. Transforming growth factor (TGF)-β and their family members have been implicated in both normal (embryonic and somatic) stem cells and CSCs. In this study, we observed that exposure to TGF-β increased the population of breast cancer (BC) cells that can form mammospheres in suspension, a feature endowed by stem cells. This was mediated by the micro (mi)RNA family miR-181, which was upregulated by TGF-β at the post-transcriptional level. Levels of the miR-181 family members were elevated in mammospheres grown in undifferentiating conditions, compared with cells grown in two-dimensional conditions. Ataxia telangiectasia mutated (ATM), a target gene of miR-181, exhibited reduced expression in mammospheres and upon TGF-β treatment. Overexpression of miR-181a/b, or depletion of ATM or its substrate CHK2, was sufficient to induce sphere formation in BC cells. Finally, knockdown of ATM enhanced in vivo tumorigenesis of the MDA361 BC cells. Our results elucidate a novel mechanism through which the TGF-β pathway regulates the CSC property by interfering with the tumor suppressor ATM, providing insights into the cellular and environmental factors regulating CSCs, which may guide future studies on therapeutic strategies targeting these cells.

Indexed as

AnimalsAtaxia Telangiectasia Mutated ProteinsBreast NeoplasmsCell Cycle ProteinsCell Line, TumorCell ShapeCheckpoint Kinase 2DNA-Binding ProteinsFemaleGene Knockdown TechniquesHumansMiceMice, Inbred NODMice, SCIDMicroRNAsNeoplastic Stem CellsAtaxia Telangiectasia Mutated ProteinsATM protein, humanAtm protein, mouseCell Cycle ProteinsCheckpoint Kinase 2CHEK2 protein, humanChek2 protein, mouseDNA-Binding ProteinsMicroRNAsMIrn181 microRNA, humanProtein Serine-Threonine KinasesTransforming Growth Factor betaTumor Suppressor Proteins

Identifiers

PMID21102523
PMCPMC3063856
OpenAlexW1996376317

What OpenQuestion holds

Textmetadata
LicenceTDM
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.