Evidence map›Paper›PMID 24867691›Full record

ArticleBritish journal of cancer2014

Connexins and cyclooxygenase-2 crosstalk in the expression of radiation-induced bystander effects.

Y Zhao, S M de Toledo, G Hu, T K Hei, E I Azzam

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

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  8. Targets for protection and mitigation of radiation injury.Cellular and molecular life sciences : CMLS · 2020
    Review
  9. Synergistic inhibitory effect of resveratrol and TK/GCV therapy on melanoma cells.Journal of cancer research and clinical oncology · 2020
    Article
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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 1 institution in 1 country.

Y ZhaoDepartment of Radiology, Rutgers University, New Jersey Medical School, Cancer Center, Newark, NJ 07103, USA.
S M de ToledoDepartment of Radiology, Rutgers University, New Jersey Medical School, Cancer Center, Newark, NJ 07103, USA.
G HuDepartment of Radiology, Rutgers University, New Jersey Medical School, Cancer Center, Newark, NJ 07103, USA.
T K HeiCenter for Radiological Research, Department of Radiation Oncology, Columbia University Medical Center, New York, NY 10032, USA.
E I AzzamDepartment of Radiology, Rutgers University, New Jersey Medical School, Cancer Center, Newark, NJ 07103, USA.
Columbia University Irving Medical Center · US

Funding

THE FUNCTIONAL GENOMICS OF BYSTANDER RESPONSESP01CA049062 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI HEI, TOM K. · 1990 to 2014
$21.9M
NCI NIH HHS CA049062NCI NIH HHS P01 CA049062
6 · The paper itself

Abstract

backgroundSignalling events mediated by connexins and cyclooxygenase-2 (COX-2) have important roles in bystander effects induced by ionising radiation. However, whether these proteins mediate bystander effects independently or cooperatively has not been investigated.

methodsBystander normal human fibroblasts were cocultured with irradiated adenocarcinoma HeLa cells in which specific connexins (Cx) are expressed in the absence of endogenous Cx, before and after COX-2 knockdown, to investigate DNA damage in bystander cells and their progeny.

resultsInducible expression of gap junctions composed of connexin26 (Cx26) in irradiated HeLa cells enhanced the induction of micronuclei in bystander cells (P<0.01) and reduced the coculture time necessary for manifestation of the effect. In contrast, expression of connexin32 (Cx32) conferred protective effects. COX-2 knockdown in irradiated HeLa Cx26 cells attenuated the bystander response due to connexin expression. However, COX-2 knockdown resulted in enhanced micronucleus formation in the progeny of the bystander cells (P<0.001). COX-2 knockdown delayed junctional communication in HeLa Cx26 cells, and reduced, in the plasma membrane, the physical interaction of Cx26 with MAPKKK, a controller of the MAPK pathway that regulates COX-2 and connexin.

conclusionsJunctional communication and COX-2 cooperatively mediate the propagation of radiation-induced non-targeted effects. Characterising the mediating events affected by both mechanisms may lead to new approaches that mitigate secondary debilitating effects of cancer radiotherapy.

Indexed as

Bystander EffectCoculture TechniquesConnexin 26ConnexinsCyclooxygenase 2FibroblastsGap JunctionsHeLa CellsHumansConnexin 26ConnexinsCyclooxygenase 2GJB2 protein, humanPTGS2 protein, human

Identifiers

PMID24867691
PMCPMC4090739
OpenAlexW2002545754

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.