Evidence map›Paper›PMID 26384430›Full record

ArticleNucleic acids research2015

CITED2 silencing sensitizes cancer cells to cisplatin by inhibiting p53 trans-activation and chromatin relaxation on the ERCC1 DNA repair gene.

Yu-Chin Liu, Pu-Yuan Chang, Chuck C-K Chao

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

17 citing papers in PubMed, 28 citations in OpenAlex.

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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

3 authors at 1 institution in 1 country.

Yu-Chin LiuTumor Biology Laboratory, Department of Biochemistry and Molecular Biology, Chang Gung University, 259 Wen-Hua first Road, Gueishan, Taoyuan 333, Taiwan, Republic of China Graduate Institute of Biomedical Sciences, Chang Gung University, 259 Wen-Hua first Road, Gueishan,Taoyuan 333, Taiwan, Republic of China.
Pu-Yuan ChangTumor Biology Laboratory, Department of Biochemistry and Molecular Biology, Chang Gung University, 259 Wen-Hua first Road, Gueishan, Taoyuan 333, Taiwan, Republic of China.
Chuck C-K ChaoTumor Biology Laboratory, Department of Biochemistry and Molecular Biology, Chang Gung University, 259 Wen-Hua first Road, Gueishan, Taoyuan 333, Taiwan, Republic of China Graduate Institute of Biomedical Sciences, Chang Gung University, 259 Wen-Hua first Road, Gueishan,Taoyuan 333, Taiwan, Republic of China cckchao@mail.cgu.edu.tw.
Chang Gung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study, we show that silencing of CITED2 using small-hairpin RNA (shCITED2) induced DNA damage and reduction of ERCC1 gene expression in HEK293, HeLa and H1299 cells, even in the absence of cisplatin. In contrast, ectopic expression of ERCC1 significantly reduced intrinsic and induced DNA damage levels, and rescued the effects of CITED2 silencing on cell viability. The effects of CITED2 silencing on DNA repair and cell death were associated with p53 activity. Furthermore, CITED2 silencing caused severe elimination of the p300 protein and markers of relaxed chromatin (acetylated H3 and H4, i.e. H3K9Ac and H3K14Ac) in HEK293 cells. Chromatin immunoprecipitation assays further revealed that DNA damage induced binding of p53 along with H3K9Ac or H3K14Ac at the ERCC1 promoter, an effect which was almost entirely abrogated by silencing of CITED2 or p300. Moreover, lentivirus-based CITED2 silencing sensitized HeLa cell line-derived tumor xenografts to cisplatin in immune-deficient mice. These results demonstrate that CITED2/p300 can be recruited by p53 at the promoter of the repair gene ERCC1 in response to cisplatin-induced DNA damage. The CITED2/p300/p53/ERCC1 pathway is thus involved in the cell response to cisplatin and represents a potential target for cancer therapy.

Indexed as

Transcriptional ActivationAnimalsAntineoplastic AgentsCell Line, TumorCell SurvivalChromatinCisplatinDNA-Binding ProteinsDNA DamageDNA RepairDown-RegulationE1A-Associated p300 ProteinEndonucleasesFemaleGene Expression Regulation, NeoplasticGene SilencingAntineoplastic AgentsChromatinCisplatinCITED2 protein, humanDNA-Binding ProteinsE1A-Associated p300 ProteinEndonucleasesEP300 protein, humanERCC1 protein, humanHistonesRepressor ProteinsRNA, MessengerTrans-ActivatorsTumor Suppressor Protein p53

Identifiers

PMID26384430
PMCPMC4678856
OpenAlexW2125638641

What OpenQuestion holds

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LicenceCC BY-NC
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.