Evidence map›Paper›PMID 34707101›Full record

ArticleScientific reports2021

NRIP1 is activated by C-JUN/C-FOS and activates the expression of PGR, ESR1 and CCND1 in luminal A breast cancer.

Renata Binato, Stephany Corrêa, Carolina Panis, Gerson Ferreira, Igor Petrone, Igor Rodrigues da Costa, Eliana Abdelhay

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

8 citing papers in PubMed, 21 citations in OpenAlex.

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  7. Epigenetic Alterations in DCIS Progression: What Can lncRNAs Teach Us?International journal of molecular sciences · 2023
    Review
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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 3 institutions in 1 country.

Renata Binato *Stem Cell Laboratory, Divisão de Laboratórios do CEMO, Bone Marrow Transplantation Unit, National Cancer Institute (INCA), Praça da Cruz Vermelha 23, 6° andar ALA C, Rio de Janeiro, RJ, CEP 20.230-130, Brazil. renata.binato@inca.gov.br.
Stephany Corrêa *Stem Cell Laboratory, Divisão de Laboratórios do CEMO, Bone Marrow Transplantation Unit, National Cancer Institute (INCA), Praça da Cruz Vermelha 23, 6° andar ALA C, Rio de Janeiro, RJ, CEP 20.230-130, Brazil.
Carolina PanisStem Cell Laboratory, Divisão de Laboratórios do CEMO, Bone Marrow Transplantation Unit, National Cancer Institute (INCA), Praça da Cruz Vermelha 23, 6° andar ALA C, Rio de Janeiro, RJ, CEP 20.230-130, Brazil.
Gerson FerreiraStem Cell Laboratory, Divisão de Laboratórios do CEMO, Bone Marrow Transplantation Unit, National Cancer Institute (INCA), Praça da Cruz Vermelha 23, 6° andar ALA C, Rio de Janeiro, RJ, CEP 20.230-130, Brazil.
Igor PetroneStem Cell Laboratory, Divisão de Laboratórios do CEMO, Bone Marrow Transplantation Unit, National Cancer Institute (INCA), Praça da Cruz Vermelha 23, 6° andar ALA C, Rio de Janeiro, RJ, CEP 20.230-130, Brazil.
Igor Rodrigues da CostaLADETEC, Departamento de Bioquímica, Instituto de Química, Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro, RJ, Brazil.
Eliana AbdelhayStem Cell Laboratory, Divisão de Laboratórios do CEMO, Bone Marrow Transplantation Unit, National Cancer Institute (INCA), Praça da Cruz Vermelha 23, 6° andar ALA C, Rio de Janeiro, RJ, CEP 20.230-130, Brazil.
Instituto Nacional do Câncer · BRUniversidade Estadual do Oeste do Paraná · BRUniversidade Federal do Rio de Janeiro · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Using chip array assays, we identified differentially expressed genes via a comparison between luminal A breast cancer subtype and normal mammary ductal cells from healthy donors. In silico analysis confirmed by western blot and immunohistochemistry revealed that C-JUN and C-FOS transcription factors are activated in luminal A patients as potential upstream regulators of these differentially expressed genes. Using a chip-on-chip assay, we identified potential C-JUN and C-FOS targets. Among these genes, the NRIP1 gene was revealed to be targeted by C-JUN and C-FOS. This was confirmed after identification and validation with transfection assays specific binding of C-JUN and C-FOS at consensus binding sites. NRIP1 is not only upregulated in luminal A patients and cell lines but also regulates breast cancer-related genes, including PR, ESR1 and CCND1. These results were confirmed by NRIP1 siRNA knockdown and chip array assays, thus highlighting the putative role of NRIP1 in PGR, ESR1 and CCND1 transcriptional regulation and suggesting that NRIP1 could play an important role in breast cancer ductal cell initiation.

Indexed as

Gene Expression Regulation, NeoplasticAdultAgedBreast NeoplasmsCarcinoma, Ductal, BreastCyclin D1Estrogen Receptor alphaFemaleHumansIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesMCF-7 CellsMiddle AgedNuclear ProteinsNuclear Receptor Interacting Protein 1Proto-Oncogene Proteins c-fosCCND1 protein, humanCyclin D1ESR1 protein, humanEstrogen Receptor alphaIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesMRFAP1 protein, humanNRIP1 protein, humanNuclear ProteinsNuclear Receptor Interacting Protein 1Proto-Oncogene Proteins c-fos

Identifiers

PMID34707101
PMCPMC8551324
OpenAlexW3208118335

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.