Evidence map›Paper›PMID 27163531›Full record

ReviewThe international journal of biochemistry & cell biology2016

Divergent modulation of normal and neoplastic stem cells by thrombospondin-1 and CD47 signaling.

Sukhbir Kaur, David D Roberts

Open access · greenAbstract readReview
In one paragraph

Review in The international journal of biochemistry & cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Functions of Thrombospondin-1 in the Tumor Microenvironment.International journal of molecular sciences · 2021
    Review
  10. CD47 (Cluster of Differentiation 47).Atlas of genetics and cytogenetics in oncology and haematology · 2021
    Article
  11. Review
  12. Review
  13. THBS1 (thrombospondin-1).Atlas of genetics and cytogenetics in oncology and haematology · 2020
    Article
  14. Article
  15. [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
  16. Review
  17. Article
  18. Article
  19. Blocking CD47-SIRPα Signal Axis as Promising Immunotherapy in Ovarian Cancer.Cancer control : journal of the Moffitt Cancer Center
    Review
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 1 institution in 1 country.

Sukhbir KaurLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, United States.
David D RobertsLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, United States. Electronic address: droberts@helix.nih.gov.
National Institutes of Health · US

Funding

Cellular Interactions with ThrombospondinZIASC009172 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI ROBERTS, DAVID D · 2009 to 2024
$17.9M
CELLULAR INTERACTIONS WITH THROMBOSPONDINZ01SC009172 · SC · DIVISION OF CLINICAL SCIENCES - NCI · PI ROBERTS, DAVID D · 1996 to 2008
$1.7M
Intramural NIH HHS Z01 SC009172
6 · The paper itself

Abstract

Thrombospondin-1 is a secreted matricellular protein that regulates the differentiation and function of many cell types. Thrombospondin-1 is not required for embryonic development, but studies using lineage-committed adult stem cells have identified positive and negative effects of thrombospondin-1 on stem cell differentiation and self-renewal and identified several thrombospondin-1 receptors that mediate these responses. Genetic studies in mice reveal a broad inhibitory role of thrombospondin-1 mediated by its receptor CD47. Cells and tissues lacking thrombospondin-1 or CD47 exhibit an increased capacity for self-renewal associated with increased expression of the stem cell transcription factors c-Myc, Sox2, Klf4, and Oct4. Thrombospondin-1 inhibits expression of these transcription factors in a CD47-dependent manner. However, this regulation differs in some neoplastic cells. Tumor initiating/cancer stem cells express high levels of CD47, but in contrast to nontransformed stem cells CD47 signaling supports cancer stem cells. Suppression of CD47 expression in cancer stem cells or ligation of CD47 by function blocking antibodies or thrombospondin-1 results in loss of self-renewal. Therefore, the therapeutic CD47 antagonists that are in clinical development for stimulating innate anti-tumor immunity may also inhibit tumor growth by suppressing cancer stem cells. These and other therapeutic modulators of thrombospondin-1 and CD47 signaling may also have applications in regenerative medicine to enhance the function of normal stem cells.

Indexed as

Signal TransductionAnimalsBone DevelopmentCD47 AntigenExtracellular MatrixHumansKruppel-Like Factor 4Neoplastic Stem CellsThrombospondin 1CD47 AntigenKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Thrombospondin 1Cancerc-MycExtracellular matrixMatricellular proteinsSelf-renewalTumor initiating cells

Identifiers

PMID27163531
PMCPMC5097897
OpenAlexW2345622380

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.