Evidence map›Paper›PMID 28594273›Full record

ArticleCell cycle (Georgetown, Tex.)2017

Effect of TPA and HTLV-1 Tax on BRCA1 and ERE controlled genes expression.

Azhar Jabareen, Aya Abu-Jaafar, Ammar Abou-Kandil, Mahmoud Huleihel

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 47% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
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

4 authors at 1 institution in 1 country.

Azhar Jabareena Shraga Segal Department of Microbiology and Immunology , Faculty of Health Sciences, Ben Gurion University of the Negev , Beer Sheva , Israel.
Aya Abu-Jaafara Shraga Segal Department of Microbiology and Immunology , Faculty of Health Sciences, Ben Gurion University of the Negev , Beer Sheva , Israel.
Ammar Abou-Kandila Shraga Segal Department of Microbiology and Immunology , Faculty of Health Sciences, Ben Gurion University of the Negev , Beer Sheva , Israel.
Mahmoud Huleihela Shraga Segal Department of Microbiology and Immunology , Faculty of Health Sciences, Ben Gurion University of the Negev , Beer Sheva , Israel.
Ben-Gurion University of the Negev · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interference with the expression and/or functions of the multifunctional tumor suppressor BRCA1 leads to a high risk of breast and ovarian cancers. BRCA1 expression is usually activated by the estrogen (E2) liganded ERα receptor. Activated ERα is considered as a potent transcription factor which activates various genes expression by 2 pathways. A classical pathway, ERα binds directly to E2-responsive elements (EREs) in the promoters of the responsive genes and a non-classical pathway where ERα indirectly binds with the appropriate gene promoter. In our previous study, HTLV-1Tax was found to strongly inhibit ERα induced BRCA1 expression while stimulating ERα induced ERE dependent genes. TPA is a strong PKC activator which found to induce the expression of HTLV-1. Here we examined the effect of TPA on the expression of BRCA1 and genes controlled by ERE region in MCF-7 cells and on Tax activity on these genes. Our results showed strong stimulatory effect of TPA on both BRCA1 and ERE expression without treatment with E2. Tax did not show any significant effect on these TPA activities. It seems that TPA activation of BRCA1 and ERE expression is dependent on PKC activity but not through the NFκB pathway. However, 53BP1 may be involved in this TPA activity because its overexpression significantly reduced the TPA stimulatory effect on BRCA1 and ERE expression. Additionally, our Chip assay results probably exclude possible involvement of ERα pathway in this TPA activity because TPA did not interfere with the binding of ERα to both BRCA1 promoter and ERE region.

Indexed as

Gene Expression Regulation, NeoplasticResponse ElementsBRCA1 ProteinEstrogen Receptor alphaFemaleGene Products, taxGenes, ReporterHost-Pathogen InteractionsHumansHuman T-lymphotropic virus 1LuciferasesMCF-7 CellsNF-kappa BPromoter Regions, GeneticSignal TransductionTetradecanoylphorbol Acetate12-O-tetradecanoylphorbol-1,3-acetateBRCA1 ProteinBRCA1 protein, humanESR1 protein, humanEstrogen Receptor alphaGene Products, taxLuciferasesNF-kappa Btax protein, Human T-lymphotrophic virus 1Tetradecanoylphorbol AcetateTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 1BRCA-1EREERαHTLV-1TaxTPA

Identifiers

PMID28594273
PMCPMC5539818
OpenAlexW2622116098

What OpenQuestion holds

Textmetadata
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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.