Evidence map›Paper›PMID 22760497›Full record

ArticleCellular and molecular life sciences : CMLS2012

CD24 controls Src/STAT3 activity in human tumors.

Niko P Bretz, Alexei V Salnikov, Claudia Perne, Sascha Keller, Xiaoli Wang, Claudia T Mierke, Mina Fogel, Natalie Erbe-Hofmann, Thomas Schlange, Gerhard Moldenhauer and 1 more

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

52 citing papers in PubMed, 80 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. CD24 flags anastasis in melanoma cells.Apoptosis : an international journal on programmed cell death · 2025
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Targeting CD24 as a novel immunotherapy for solid cancers.Cell communication and signaling : CCS · 2023
    Review
  14. Emerging Immune Checkpoint Molecules on Cancer Cells: CD24 and CD200.International journal of molecular sciences · 2023
    Review
  15. Article
  16. Article
  17. Review
  18. Surprising magic of CD24 beyond cancer.Frontiers in immunology · 2023
    Review
  19. Review
  20. CD24: A Novel Target for Cancer Immunotherapy.Journal of personalized medicine · 2022
    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

11 authors at 5 institutions in 2 countries.

Niko P BretzTumor Immunology Programme, German Cancer Research Center, Heidelberg, Germany.
Alexei V Salnikov
Claudia Perne
Sascha Keller
Xiaoli Wang
Claudia T Mierke
Mina Fogel
Natalie Erbe-Hofmann
Thomas Schlange
Gerhard Moldenhauer
Peter Altevogt
German Cancer Research Center · DEHeidelberg University · DEBayer (Germany) · DEKaplan Medical Center · ILLeipzig University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD24 is a glycosyl-phosphatidylinositol-anchored membrane protein that is frequently over-expressed in a variety of human carcinomas and is correlated with poor prognosis. In cancer cell lines, changes of CD24 expression can alter several cellular properties in vitro and tumor growth in vivo. However, little is known about how CD24 mediates these effects. Here we have analyzed the functional consequences of CD24 knock-down or over-expression in human cancer cell lines. Depletion of CD24 reduced cell proliferation and adhesion, enhanced apoptosis, and regulated the expression of various genes some of which were identified as STAT3 target genes. Loss of CD24 reduced STAT3 and FAK phosphorylation. Diminished STAT3 activity was confirmed by specific reporter assays. We found that reduced STAT3 activity after CD24 knock-down was accompanied by altered Src phosphorylation. Silencing of Src, similar to CD24, targeted the expression of prototype STAT3-regulated genes. Likewise, the over-expression of CD24 augmented Src-Y416 phosphorylation, the recruitment of Src into lipid rafts and the expression of STAT3-dependent target genes. An antibody to CD24 was effective in reducing tumor growth of A549 lung cancer and BxPC3 pancreatic cancer xenografts in mice. Antibody treatment affected the level of Src-phosphorylation in the tumor and altered the expression of STAT3 target genes. Our results provide evidence that CD24 regulates STAT3 and FAK activity and suggest an important role of Src in this process. Finally, the targeting of CD24 by antibodies could represent a novel route for tumor therapy.

Indexed as

AnimalsAntibodies, MonoclonalApoptosisCD24 AntigenCell AdhesionCell Line, TumorCell ProliferationFocal Adhesion Kinase 1Gene Expression RegulationHumansMiceMice, Inbred NODMice, SCIDNeoplasmsNeoplasm TransplantationPhosphorylationAntibodies, MonoclonalCD24 AntigenFocal Adhesion Kinase 1PTK2 protein, humanRNA, Small Interferingsrc-Family KinasesSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID22760497
PMCPMC11114558
OpenAlexW2085105893

What OpenQuestion holds

Textmetadata
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.