Evidence map›Paper›PMID 21268715›Full record

ArticleRadiation research2011

The mTOR inhibitor rapamycin suppresses DNA double-strand break repair.

Honghong Chen, Zhefu Ma, Robert P Vanderwaal, Zhihui Feng, Ignacio Gonzalez-Suarez, Shenming Wang, Jiuqin Zhang, Joseph L Roti Roti, Susana Gonzalo, Junran Zhang

Open access · greenAbstract read
In one paragraph

Article in Radiation research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
3.5field-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

68 citing papers in PubMed, 95 citations in OpenAlex.

  1. Review
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  4. New approaches to overcome radioresistance in glioblastoma: mechanisms, targets and role of innovative therapies, new particles and non-photon radiotherapy in 2024. A systematic review.Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 2025
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  17. Modulation of mTOR signaling by radiation and rapamycin treatment in canine mast cell cancer cells.Canadian journal of veterinary research = Revue canadienne de recherche veterinaire · 2022
    Article
  18. OGG1 in the Kidney: Beyond Base Excision Repair.Oxidative medicine and cellular longevity · 2022
    Review
  19. Article
  20. Article

8 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

10 authors at 3 institutions in 2 countries.

Honghong ChenDepartment of Radiation Oncology, Washington University School of Medicine, 4511 Forest Park Blvd., St. Louis, MO 63108, USA.
Zhefu Ma
Robert P Vanderwaal
Zhihui Feng
Ignacio Gonzalez-Suarez
Shenming Wang
Jiuqin Zhang
Joseph L Roti Roti
Susana Gonzalo
Junran Zhang
Washington University in St. Louis · USSun Yat-sen University · CNThe First Affiliated Hospital, Sun Yat-sen University · CN

Funding

MECHANISMS RESPONSIBLE FOR GENOMIC INSTABILITY IN PREMATURE AGING LAMINOPATHIESR01GM094513 · NIGMS · WASHINGTON UNIVERSITY · PI GONZALO HERVAS, SUSANA · 2010 to 2014
$1.4M
NIGMS NIH HHS R01 GM094513
6 · The paper itself

Abstract

mTOR (mammalian target of rapamycin) signaling plays a key role in the development of many tumor types. Therefore, mTOR is an attractive target for cancer therapeutics. Although mTOR inhibitors are thought to have radiosensitization activity, the molecular bases remain largely unknown. Here we show that treating MCF7 breast cancer cells with rapamycin (an mTOR inhibitor) results in significant suppression of homologous recombination (HR) and nonhomologous end joining (NHEJ), two major mechanisms required for repairing ionizing radiation-induced DNA DSBs. We observed that rapamycin impaired recruitment of BRCA1 and Rad51 to DNA repair foci, both essential for HR. Moreover, consistent with the suppressive role of rapamycin on both HR and NHEJ, persistent radiation-induced DSBs were detected in cells pretreated with rapamycin. Furthermore, the frequency of chromosome and chromatid breaks was increased in cells treated with rapamycin before and after irradiation. Thus our results show that radiosensitization by mTOR inhibitors occurs via disruption of the major two DNA DSB repair pathways.

Indexed as

DNA Breaks, Double-StrandedBRCA1 ProteinBreast NeoplasmsCell Line, TumorChromosome AberrationsDNA RepairFemaleHumansRad51 RecombinaseRecombination, GeneticSirolimusTOR Serine-Threonine KinasesBRCA1 ProteinBRCA1 protein, humanRAD51 protein, humanRad51 RecombinaseSirolimusTOR Serine-Threonine Kinases

Identifiers

PMID21268715
PMCPMC4412148
OpenAlexW2013807892

What OpenQuestion holds

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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.