Evidence map›Paper›PMID 23730208›Full record

ArticleNeoplasia (New York, N.Y.)2013

BRCA1 expression is epigenetically repressed in sporadic ovarian cancer cells by overexpression of C-terminal binding protein 2.

Taymaa May, Junzheng Yang, Melina Shoni, Shubai Liu, Housheng He, Reddy Gali, Shu-Kay Ng, Christopher Crum, Ross S Berkowitz, Shu-Wing Ng

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

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  12. MicroRNA485-3p negatively regulates the transcriptional co-repressorInternational journal of biological sciences · 2018
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  19. Effect of adriamycin on BRCA1 and PARP-1 expression in MCF-7 breast cancer cells.International journal of clinical and experimental pathology · 2014
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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

10 authors at 3 institutions in 2 countries.

Taymaa MayDepartment of Obstetrics/Gynecology and Reproductive Biology, Division of Gynecologic Oncology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Junzheng Yang
Melina Shoni
Shubai Liu
Housheng He
Reddy Gali
Shu-Kay Ng
Christopher Crum
Ross S Berkowitz
Shu-Wing Ng
Brigham and Women's Hospital · USGriffith University · AUHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionOvarian cancer is the leading cause of mortality from gynecological malignancy despite advancements in novel therapeutics. We have recently demonstrated that the transcriptional co-repressor C-terminal binding protein 2 (CtBP2) is overexpressed in epithelial ovarian carcinoma. MATERIALS AND

methodsReverse-transcribed cDNA from CtBP2 wild-type and knockdown ovarian cancer cell lines was hybridized to Affymetrix Gene 1.0 ST microarrays, and differentially expressed genes were studied. Immunohistochemical analysis of CtBP2 and BRCA1 staining of ovarian tissues was performed. Chromatin immunoprecipitation (ChIP) and luciferase assays were carried out. The effect of the drugs 4-methylthio-2-oxobutyric acid (MTOB) and poly(ADP-ribose) polymerase (PARP) inhibitor Olaparib on CtBP2 wild-type and knockdown cell lines was examined using methylthiazol tetrazolium assays and an xCELLigence System.

resultsEighty-five genes involved in DNA repair, mitotic checkpoint, nucleosome assembly, and the BRCA1 network were differentially regulated by CtBP2 expression. ChIP and luciferase reporter assays using a BRCA1 promoter-regulated luciferase construct indicated that the CtBP2 complex binds the BRCA1 promoter and represses BRCA1 transcription. Immunohistochemistry illustrated a significant inverse CtBP2 and BRCA1 expression in a panel of malignant ovarian tumor tissues. The CtBP2 inhibitor MTOB suppressed ovarian cancer cell survival in a CtBP2-dependent manner. Ovarian cancer cells with CtBP2 knockdown did not display increased sensitivity to the PARP inhibitor Olaparib.

conclusionCtBP2 is an ovarian cancer oncogene that may play a significant role in epigenetically silencing BRCA1 function in sporadic epithelial ovarian cancer. CtBP2-specific inhibitors, such as MTOB, may be effective adjunct therapies in the management of patients with CtBP2-positive ovarian carcinoma.

Indexed as

Epigenesis, GeneticGene Expression Regulation, NeoplasticAlcohol OxidoreductasesBRCA1 ProteinCarcinoma, Ovarian EpithelialCell Line, TumorCell SurvivalCo-Repressor ProteinsFemaleGene Expression ProfilingGene Knockdown TechniquesHumansMethionineNeoplasms, Glandular and EpithelialNerve Tissue ProteinsOvarian Neoplasms2-keto-4-methylthiobutyric acidAlcohol OxidoreductasesBRCA1 ProteinBRCA1 protein, humanCo-Repressor ProteinsCTBP2 protein, humanMethionineNerve Tissue ProteinsolaparibPhthalazinesPiperazinesPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) Polymerases

Identifiers

PMID23730208
PMCPMC3664992
OpenAlexW1241198455

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.