Evidence map›Paper›PMID 26049366›Full record

ArticleMolecular and cellular biochemistry2015

The involvement of c-Myc in the DNA double-strand break repair via regulating radiation-induced phosphorylation of ATM and DNA-PKcs activity.

Fengmei Cui, Rong Fan, Qiu Chen, Yongming He, Man Song, Zengfu Shang, Shimeng Zhang, Wei Zhu, Jianping Cao, Hua Guan and 1 more

Abstract read
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Article in Molecular and cellular biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

28 citing papers in PubMed, 42 citations in OpenAlex.

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  11. Unraveling MYC's Role in Orchestrating Tumor Intrinsic and Tumor Microenvironment Interactions Driving Tumorigenesis and Drug Resistance.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023
    Review
  12. Role of c-Myc in lung cancer: Progress, challenges, and prospects.Chinese medical journal pulmonary and critical care medicine · 2023
    Article
  13. Article
  14. Article
  15. Article
  16. Review
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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

11 authors at 4 institutions in 1 country.

Fengmei CuiDepartment of Radiation Medicine, School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou, 215123, China.
Rong Fan
Qiu Chen
Yongming He
Man Song
Zengfu Shang
Shimeng Zhang
Wei Zhu
Jianping Cao
Hua Guan
Ping-Kun Zhou
Soochow University · CNBeijing Radiation Center · CNFirst Affiliated Hospital of Soochow University · CNLogistics University of People's Armed Police Force · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deregulation of c-Myc often occurs in various human cancers, which not only contributes to the genesis and progression of cancers but also affects the outcomes of cancer radio- or chemotherapy. In this study, we have investigated the function of c-Myc in the repair of DNA double-strand break (DSB) induced by γ-ray irradiation. A c-Myc-silenced Hela-630 cell line was generated from HeLa cells using RNA interference technology. The DNA DSBs were detected by γ-H2AX foci, neutral comet assay and pulsed-field gel electrophoresis. We found that the capability of DNA DSB repair in Hela-630 cells was significantly reduced, and the repair kinetics of DSB was delayed as compared to the control Hela-NC cells. Silence of c-myc sensitized the cellular sensitivity to ionizing radiation. The phosphorylated c-Myc (Thr58/pSer62) formed the consistent co-localisation foci with γ-H2AX as well as the phosphorylated DNA-PKcs/S2056 in the irradiated cells. Moreover, depression of c-Myc largely attenuated the ionizing radiation-induced phosphorylation of the ataxia telangiectasia mutated (ATM) and decreased the in vitro kinase activity of DNA-PKcs. Taken together, our results demonstrated that c-Myc protein functions in the process of DNA double-strand break repair, at least partially, through affecting the ATM phosphorylation and DNA-PKcs kinase activity. The overexpression of c-Myc in tumours can account for the radioresistance of some tumour cell types.

Indexed as

DNA RepairAtaxia Telangiectasia Mutated ProteinsCell ProliferationDNA-Activated Protein KinaseDNA Breaks, Double-StrandedHeLa CellsHumansNuclear ProteinsPhosphorylationProtein Processing, Post-TranslationalProto-Oncogene Proteins c-mycAtaxia Telangiectasia Mutated ProteinsATM protein, humanDNA-Activated Protein KinaseMYC protein, humanNuclear ProteinsPRKDC protein, humanProto-Oncogene Proteins c-myc

Identifiers

PMID26049366
OpenAlexW630412634

What OpenQuestion holds

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Registered trials

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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.