Evidence map›Paper›PMID 27895503›Full record

ArticleOncoTargets and therapy2016

Methotrexate induces DNA damage and inhibits homologous recombination repair in choriocarcinoma cells.

Lisha Xie, Tiancen Zhao, Jing Cai, You Su, Zehua Wang, Weihong Dong

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
5.2field-weighted citation impact, top 5% 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

22 citing papers in PubMed, 33 citations in OpenAlex.

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  16. Targeting Nuclear NADCancers · 2020
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  19. Canonical Wnt is inhibited by targeting one-carbon metabolism through methotrexate or methionine deprivation.Proceedings of the National Academy of Sciences of the United States of America · 2019
    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

6 authors at 3 institutions in 2 countries.

Lisha XieDepartment of Obstetrics and Gynecology, Union Hospital,Tongji Medical College, Huazhong University of Science and Technology.
Tiancen ZhaoDepartment of Obstetrics and Gynecology, Union Hospital,Tongji Medical College, Huazhong University of Science and Technology; Department of Obstetrics and Gynecology, Central Hospital of Wuhan, Wuhan, China.
Jing CaiDepartment of Obstetrics and Gynecology, Union Hospital,Tongji Medical College, Huazhong University of Science and Technology.
You SuDepartment of Obstetrics and Gynecology, Union Hospital,Tongji Medical College, Huazhong University of Science and Technology.
Zehua WangDepartment of Obstetrics and Gynecology, Union Hospital,Tongji Medical College, Huazhong University of Science and Technology.
Weihong DongDepartment of Obstetrics and Gynecology, Union Hospital,Tongji Medical College, Huazhong University of Science and Technology.
Union Hospital · USHuazhong University of Science and Technology · CNCentral Hospital of Wuhan · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe objective of this study was to investigate the mechanism of sensitivity to methotrexate (MTX) in human choriocarcinoma cells regarding DNA damage response.

methodsTwo choriocarcinoma cancer cell lines, JAR and JEG-3, were utilized in this study. An MTX-sensitive osteosarcoma cell line MG63, an MTX-resistant epithelial ovarian cancer cell line A2780 and an MTX-resistant cervical adenocarcinoma cell line Hela served as controls. Cell viability assay was carried out to assess MTX sensitivity of cell lines. MTX-induced DNA damage was evaluated by comet assay. Quantitative reverse transcription polymerase chain reaction was used to detect the mRNA levels of BRCA1, BRCA2, RAD51 and RAD52. The protein levels of γH2AX, RAD 51 and p53 were analyzed by Western blot.

resultsRemarkable DNA strand breaks were observed in MTX-sensitive cell lines (JAR, JEG-3 and MG63) but not in MTX-resistant cancer cells (A2780 and Hela) after 48 h of MTX treatment. Only in the choriocarcinoma cells, the expression of homologous recombination (HR) repair gene RAD51 was dramatically suppressed by MTX in a dose- and time-dependent manner, accompanied with the increase in p53.

conclusionThe MTX-induced DNA strand breaks accompanied by deficiencies in HR repair may contribute to the hypersensitivity to chemotherapy in choriocarcinoma.

Indexed as

chemotherapy hypersensitivitychoriocarcinomaDNA double-strand breakp53RAD51

Identifiers

PMID27895503
PMCPMC5119623
OpenAlexW2551195572

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.