Evidence map›Paper›PMID 33547534›Full record

ArticleMolecular biology reports2021

5-Aza-2'-deoxycytidine induces a greater inflammatory change, at the molecular levels, in normoxic than hypoxic tumor microenvironment.

Ísis Salviano Soares de Amorim, Juliana Alves Rodrigues, Pedro Nicolau, Sandra König, Carolina Panis, Adenilson de Souza da Fonseca, Andre Luiz Mencalha

Abstract read
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In one paragraph

Article in Molecular biology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 51% 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

4 citing papers in PubMed, 6 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

7 authors at 4 institutions in 1 country.

Ísis Salviano Soares de AmorimLaboratório de Biologia do Câncer, Instituto de Biologia Roberto Alcântara Gomes, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, RJ, Brazil.ORCID http://orcid.org/0000-0002-2762-1400
Juliana Alves RodriguesLaboratório de Biologia do Câncer, Instituto de Biologia Roberto Alcântara Gomes, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, RJ, Brazil.ORCID http://orcid.org/0000-0002-4139-4080
Pedro NicolauPrograma de Carcinogênese Molecular, Instituto Nacional de Câncer, Rio de Janeiro, RJ, Brazil.ORCID http://orcid.org/0000-0003-3322-2120
Sandra KönigDepartamento de Anatomia, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brazil.ORCID http://orcid.org/0000-0002-9400-076X
Carolina PanisLaboratório de Biologia de Tumores, Universidade Estadual do Oeste do Paraná, UNIOESTE, Francisco Beltrão, PR, Brazil.ORCID http://orcid.org/0000-0002-0104-4369
Adenilson de Souza da FonsecaLaboratório de Biologia do Câncer, Instituto de Biologia Roberto Alcântara Gomes, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, RJ, Brazil.ORCID http://orcid.org/0000-0002-4441-4008
Andre Luiz MencalhaLaboratório de Biologia do Câncer, Instituto de Biologia Roberto Alcântara Gomes, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, RJ, Brazil. andre.mencalha@uerj.br.ORCID http://orcid.org/0000-0003-3229-8094
Universidade do Estado do Rio de Janeiro · BRInstituto Nacional de Câncer - INCA · BRUniversidade Estadual do Oeste do Paraná · BRUniversidade Federal do Rio de Janeiro · BR

Funding

Conselho Nacional de Desenvolvimento Científico e Tecnológico 302505/2018-0Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro E-26/010.100944/2018
6 · The paper itself

Abstract

Hypoxia is associated with tumor aggressiveness and poor prognosis, including breast cancer. Low oxygen levels induces global genomic hypomethylation and hypermethylation of specific loci in tumor cells. DNA methylation is a reversible epigenetic modification, usually associated with gene silencing, contributing to carcinogenesis and tumor progression. Since the effects of DNA methyltransferase inhibitor are context-dependent and as there is little data comparing their molecular effects in normoxic and hypoxic microenvironments in breast cancer, this study aimed to understand the gene expression profiles and molecular effects in response to treatment with DNA methyltransferase inhibitor in normoxia and hypoxia, using the breast cancer model. For this, a cDNA microarray was used to analyze the changes in the transcriptome upon treatment with DNA methyltransferase inhibitor (5-Aza-2'-deoxycytidine: 5-Aza-2'-dC), in normoxia and hypoxia. Furthermore, immunocytochemistry was performed to investigate the effect of 5-Aza-2'-dC on NF-κB/p65 inflammation regulator subcellular localization and expression, in normoxia and hypoxia conditions. We observed that proinflammatory pathways were upregulated by treatment with 5-Aza-2'-dC, in both conditions. However, treatment with 5-Aza-2'-dC in normoxia showed a greater amount of overexpressed proinflammatory pathways than 5-Aza-2'-dC in hypoxia. In this sense, we observed that the NF-κB expression increased only upon 5-Aza-2'-dC in normoxia. Moreover, nuclear staining for NF-κB and NF-κB target genes upregulation, IL1A and IL1B, were also observed after 5-Aza-2'-dC in normoxia. Our results suggest that 5-Aza-2'-dC induces a greater inflammatory change, at the molecular levels, in normoxic than hypoxic tumor microenvironment. These data may support further studies and expand the understanding of the DNA methyltransferase inhibitor effects in different tumor contexts.

Indexed as

AcetylationCell Line, TumorDecitabineDNA MethylationDNA Modification MethylasesEnzyme InhibitorsEpigenesis, GeneticHumansInflammationPromoter Regions, GeneticTranscription Factor RelATumor HypoxiaTumor MicroenvironmentDecitabineDNA Modification MethylasesEnzyme InhibitorsRELA protein, humanTranscription Factor RelA5-Aza-2’-deoxycytidineHypoxiaInflammationNormoxiaTranscritome

Identifiers

PMID33547534
OpenAlexW3126423778

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.