Evidence map›Paper›PMID 16247454›Full record

ArticleOncogene2006

beta1-integrin-mediated signaling essentially contributes to cell survival after radiation-induced genotoxic injury.

N Cordes, J Seidler, R Durzok, H Geinitz, C Brakebusch

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

77 citing papers in PubMed, 150 citations in OpenAlex.

  1. Beyond DNA damage: 3D tumor models and the integrin mechanobiology of radioresistance.Journal of experimental & clinical cancer research : CR · 2026
    Review
  2. Review
  3. Advances in molecular targeted therapies to increase efficacy of (chemo)radiation therapy.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2023
    Review
  4. Review
  5. Article
  6. Effect of mechanical forces on cellular response to radiation.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2022
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Wee1 Kinase: A Potential Target to Overcome Tumor Resistance to Therapy.International journal of molecular sciences · 2021
    Review
  15. Review
  16. Review
  17. Extracellular matrix and its therapeutic potential for cancer treatment.Signal transduction and targeted therapy · 2021
    Review
  18. Article
  19. Review
  20. Review

17 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

5 authors at 3 institutions in 1 country.

N CordesOncoRay -- Radiation Research in Oncology, Medical Faculty Carl Gustav Carus, Technical University Dresden, Fetscherstrasse, Dresden, Germany. Nils.Cordes@mailbox.tu-dresden.de
J Seidler
R Durzok
H Geinitz
C Brakebusch
OncoRay · DEKlinikum rechts der Isar · DEMax Planck Institute of Biochemistry · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Integrin-mediated adhesion to extracellular matrix proteins confers resistance to radiation- or drug-induced genotoxic injury. To analyse the underlying mechanisms specific for beta1-integrins, wild-type beta1A-integrin-expressing GD25beta1A cells were compared to GD25beta1B cells, which express signaling-incompetent beta1B variants. Cells grown on fibronectin, collagen-III, beta1-integrin-IgG or poly-l-lysine were exposed to 0-6 Gy X-rays in presence or depletion of growth factors and phosphatidylinositol-3 kinase (PI3K) inhibitors (LY294002, wortmannin). In order to test the relevance of these findings in tumor cells, human A-172 glioma cells were examined under the same conditions after siRNA-mediated silencing of beta1-integrins. We found that beta1A-integrin-mediated adhesion to fibronectin, collagen-III or beta1-IgG was essential for cell survival after radiation-induced genotoxic injury. Mediated by PI3K, pro-survival beta1A-integrin/Akt signaling was critically involved in this process. Additionally, the beta1-integrin downstream targets p130Cas and paxillin-impaired survival-regulating PI3K-dependent JNK. In A-172 glioma cells, beta1-integrin knockdown and PI3K inhibition confirmed the central role of beta1-integrins in Akt- and p130Cas/paxillin-mediated prosurvival signaling. These findings suggest beta1-integrins as critical regulators of cell survival after radiation-induced genotoxic injury. Elucidation of the molecular circuitry of prosurvival beta1-integrin-mediated signaling in tumor cells may promote the development of innovative molecular-targeted therapeutic antitumor strategies.

Indexed as

Cell SurvivalRadiation InjuriesAnimalsBrain NeoplasmsCell AdhesionCell Culture TechniquesExtracellular Matrix ProteinsFibroblastsFibronectinsGliomaGrowth SubstancesHumansIntegrin beta1MiceProto-Oncogene Proteins c-aktRNA, Small InterferingExtracellular Matrix ProteinsFibronectinsGrowth SubstancesIntegrin beta1Proto-Oncogene Proteins c-aktRNA, Small Interfering

Identifiers

PMID16247454
OpenAlexW2031648890

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.