Evidence map›Paper›PMID 27431580›Full record

ArticleInternational journal of oncology2016

Dexamethasone downregulates expression of carbonic anhydrase IX via HIF-1α and NF-κB-dependent mechanisms.

Veronika Simko, Martina Takacova, Michaela Debreova, Katarina Laposova, Elena Ondriskova-Panisova, Silvia Pastorekova, Lucia Csaderova, Jaromir Pastorek

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

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  6. Is carbonic anhydrase inhibition useful as a complementary therapy of Covid-19 infection?Journal of enzyme inhibition and medicinal chemistry · 2021
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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

8 authors at 2 institutions in 1 country.

Veronika SimkoInstitute of Virology, Biomedical Research Center, Slovak Academy of Sciences, Bratislava, Slovak Republic.
Martina TakacovaInstitute of Virology, Biomedical Research Center, Slovak Academy of Sciences, Bratislava, Slovak Republic.
Michaela DebreovaInstitute of Virology, Biomedical Research Center, Slovak Academy of Sciences, Bratislava, Slovak Republic.
Katarina LaposovaInstitute of Virology, Biomedical Research Center, Slovak Academy of Sciences, Bratislava, Slovak Republic.
Elena Ondriskova-PanisovaInstitute of Virology, Biomedical Research Center, Slovak Academy of Sciences, Bratislava, Slovak Republic.
Silvia PastorekovaInstitute of Virology, Biomedical Research Center, Slovak Academy of Sciences, Bratislava, Slovak Republic.
Lucia CsaderovaInstitute of Virology, Biomedical Research Center, Slovak Academy of Sciences, Bratislava, Slovak Republic.
Jaromir PastorekInstitute of Virology, Biomedical Research Center, Slovak Academy of Sciences, Bratislava, Slovak Republic.
Institute of Virology of the Slovak Academy of Sciences · SKBiomedical Research Center of the Slovak Academy of Sciences · SK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dexamethasone is a synthetic glucocorticoid frequently used to suppress side-effects of anticancer chemotherapy. In the present study, we showed that dexamethasone treatment leads to concentration-dependent downregulation of cancer-associated marker, carbonic anhydrase IX (CA IX), at the level of promoter activity, mRNA and protein expression in 2D and 3D cancer cell models. The effect of dexamethasone on CA IX expression under hypoxic conditions is predominantly mediated by impaired transcriptional activity and decreased protein level of the main hypoxic transcription factor HIF-1α. In addition, CA9 downregulation can be caused by protein-protein interactions between activated glucocorticoid receptors, major effectors of glucocorticoid action, and transcription factors that trigger CA9 transcription (e.g. AP-1). Moreover, we identified a potential NF-κB binding site in the CA9 promoter and propose the involvement of NF-κB in the dexamethasone-mediated inhibition of CA9 transcription. As high level of CA IX is often linked to aggressive tumor behavior, poor prognosis and chemo- and radiotherapy resistance, uncovering its reduction after dexamethasone treatment and implication of additional regulatory mechanisms can be relevant for the CA IX-related clinical applications.

Indexed as

Down-RegulationAntigens, NeoplasmBinding SitesCarbonic Anhydrase IXCell HypoxiaCell Line, TumorCell ProliferationDexamethasoneDose-Response Relationship, DrugGlucocorticoidsHumansHypoxia-Inducible Factor 1, alpha SubunitMCF-7 CellsNF-kappa BPromoter Regions, GeneticSpheroids, CellularAntigens, NeoplasmCA9 protein, humanCarbonic Anhydrase IXDexamethasoneGlucocorticoidsHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitNF-kappa B

Identifiers

PMID27431580
PMCPMC5021256
OpenAlexW2465286361

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.