Evidence map›Paper›PMID 25109329›Full record

ArticleOncogene2015

Thrombospondin-1 repression is mediated via distinct mechanisms in fibroblasts and epithelial cells.

R S Watnick, R K Rodriguez, S Wang, A L Blois, A Rangarajan, T Ince, R A Weinberg

RetractedErratum issuedOpen access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 32 citations in OpenAlex.

  1. The theory of tumor ecosystem.Cancer communications (London, England) · 2022
    Review
  2. Review
  3. Article
  4. Review
  5. [Relationship between thrombospondin-1 and the occurrence and development of oral and maxillofacial malignancy].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2018
    Review
  6. Hepato-entrained B220EMBO molecular medicine · 2018
    Article
  7. Article
  8. Review
  9. Divergent modulation of normal and neoplastic stem cells by thrombospondin-1 and CD47 signaling.The international journal of biochemistry & cell biology · 2016
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

R S Watnick1] Vascular Biology Program, Boston Children's Hospital, Boston, MA, USA [2] Department of Surgery, Harvard Medical School, Boston, MA, USA [3] Whitehead Institute for Biomedical Research, Cambridge, MA, USA.
R K Rodriguez1] Vascular Biology Program, Boston Children's Hospital, Boston, MA, USA [2] Department of Surgery, Harvard Medical School, Boston, MA, USA [3] Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA.
S WangVascular Biology Program, Boston Children's Hospital, Boston, MA, USA.
A L Blois1] Vascular Biology Program, Boston Children's Hospital, Boston, MA, USA [2] Centre for Cancer Biomarkers CCBIO, Department of Clinical Medicine, Faculty of Medicine, University of Bergen, Bergen, Norway.
A RangarajanWhitehead Institute for Biomedical Research, Cambridge, MA, USA.
T InceWhitehead Institute for Biomedical Research, Cambridge, MA, USA.
R A Weinberg1] Whitehead Institute for Biomedical Research, Cambridge, MA, USA [2] Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA.
Boston Children's Hospital · USWhitehead Institute for Biomedical Research · US

Funding

Induced Differentiation to Deplete CSCs from Breast CancerR01CA078461 · NCI · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI WEINBERG, ROBERT A · 1999 to 2017
$8.5M
NCI NIH HHS 5 R01CA78461NCI NIH HHS R01 CA078461
6 · The paper itself

Abstract

Tumor-associated angiogenesis is postulated to be regulated by the balance between pro- and anti-angiogenic factors. We demonstrate here that the critical step in establishing the angiogenic capability of human tumor cells is the repression of a key secreted anti-angiogenic factor, thrombospondin-1 (Tsp-1). This repression is essential for tumor formation by mammary epithelial cells and kidney cells engineered to express SV40 early region proteins, hTERT, and H-RasV12. In transformed epithelial cells, a signaling pathway leading from Ras to Tsp-1 repression induces the sequential activation of PI3 kinase, Rho and ROCK, leading to activation of Myc through phosphorylation, thereby enabling Myc to repress Tsp-1 transcription. In transformed fibroblasts, however, the repression of Tsp-1 can be achieved by an alternative mechanism involving inactivation of both p53 and pRb. We thus describe novel mechanisms by which the activation of oncogenes in epithelial cells and the inactivation of tumor suppressors in fibroblasts permits angiogenesis and, in turn, tumor formation.

Indexed as

Cells, CulturedDown-RegulationE2F1 Transcription FactorEpithelial CellsFibroblastsHumansNeovascularization, PathologicPhosphatidylinositol 3-Kinasesras ProteinsRetinoblastoma ProteinSignal TransductionThrombospondin 1Tumor Suppressor Protein p53E2F1 protein, humanE2F1 Transcription FactorPhosphatidylinositol 3-Kinasesras ProteinsRetinoblastoma ProteinThrombospondin 1TP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID25109329
PMCPMC6293990
OpenAlexW2016639588

What OpenQuestion holds

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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.