Evidence map›Paper›PMID 11526489›Full record

ArticleOncogene2001

Ionizing radiation but not anticancer drugs causes cell cycle arrest and failure to activate the mitochondrial death pathway in MCF-7 breast carcinoma cells.

R U Jänicke, I H Engels, T Dunkern, B Kaina, K Schulze-Osthoff, A G Porter

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

30 citing papers in PubMed, 81 citations in OpenAlex.

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  7. Bicalutamide enhances fodrin-mediated apoptosis through calpain in LNCaP.Experimental biology and medicine (Maywood, N.J.) · 2018
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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

6 authors at 3 institutions in 2 countries.

R U JänickeDepartment of Immunology and Cell Biology, University of Münster, Röntgenstrasse 21, 48149 Münster, Germany. r.janicke@uni-muenster.de
I H Engels
T Dunkern
B Kaina
K Schulze-Osthoff
A G Porter
University of Münster · DEJohannes Gutenberg University Mainz · DEInstitute of Molecular and Cell Biology · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is considerable evidence that ionizing radiation (IR) and chemotherapeutic drugs mediate apoptosis through the intrinsic death pathway via the release of mitochondrial cytochrome c and activation of caspases -9 and -3. Here we show that MCF-7 cells that lack caspase-3 undergo a caspase-dependent apoptotic cell death in the absence of DNA fragmentation and alpha-fodrin cleavage following treatment with etoposide or doxorubicin, but not after exposure to IR. Re-expression of caspase-3 restored DNA fragmentation and alpha-fodrin cleavage following drug treatment, but it did not alter the radiation-resistant phenotype of these cells. In contrast to the anticancer drugs, IR failed to induce the intrinsic death pathway in MCF-7/casp-3 cells, an event readily observed in IR-induced apoptosis of HeLa cells. Although IR-induced DNA double-strand breaks were repaired with similar efficiencies in all cell lines, cell cycle analyses revealed a persistent G2/M arrest in the two MCF-7 cell lines, but not in HeLa cells. Together, our data demonstrate that caspase-3 is required for DNA fragmentation and alpha-fodrin cleavage in drug-induced apoptosis and that the intrinsic death pathway is fully functional in MCF-7 cells. Furthermore, they show that the radiation-resistant phenotype of MCF-7 cells is not due to the lack of caspase-3, but is caused by the failure of IR to activate the intrinsic death pathway. We propose (1) different signaling pathways are induced by anticancer drugs and IR, and (2) IR-induced G2/M arrest prevents the generation of an apoptotic signal required for the activation of the intrinsic death pathway.

Indexed as

ApoptosisRadiation, IonizingAntineoplastic AgentsBreast NeoplasmsCarcinomaCarrier ProteinsCaspase 3Caspase 9CaspasesCell CycleDNA DamageDNA FragmentationDNA, NeoplasmDoxorubicinEtoposideFemaleAntineoplastic AgentsCarrier ProteinsCASP3 protein, humanCASP9 protein, humanCaspase 3Caspase 9CaspasesDNA, NeoplasmDoxorubicinEtoposideMicrofilament ProteinsSpectrin

Identifiers

PMID11526489
OpenAlexW2321119724

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.