Evidence map›Paper›PMID 38522065›Full record

ArticleBiochemical genetics2025

Enhancing RECK Expression Through miR-21 Inhibition: A Promising Strategy for Bladder Carcinoma Control.

Paulo Rodolfo Moraes Dos Santos, Paulo Ricardo da Silva Gomes, Poliana Romão, Feres Camargo Maluf, Vanessa Ribeiro Guimarães, Patrícia Candido, Guilherme Lopes Gonçalves, Juliana Alves de Camargo, Gabriel Arantes Dos Santos, Iran Silva and 5 more

Abstract read
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In one paragraph

Article in Biochemical genetics, 2025. 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
1.7field-weighted citation impact, top 16% 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.

  1. Article
  2. Review
  3. Review
  4. 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

15 authors at 5 institutions in 2 countries.

Paulo Rodolfo Moraes Dos SantosLaboratorio de Investigação Médica 55 (LIM55), Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, SP, Brazil.
Paulo Ricardo da Silva GomesLaboratorio de Investigação Médica 55 (LIM55), Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, SP, Brazil.
Poliana RomãoLaboratorio de Investigação Médica 55 (LIM55), Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, SP, Brazil.
Feres Camargo MalufLaboratorio de Investigação Médica 55 (LIM55), Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, SP, Brazil.
Vanessa Ribeiro GuimarãesLaboratorio de Investigação Médica 55 (LIM55), Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, SP, Brazil.
Patrícia CandidoLaboratorio de Investigação Médica 55 (LIM55), Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, SP, Brazil.
Guilherme Lopes GonçalvesLaboratory of Renal Physiology, Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
Juliana Alves de CamargoLaboratorio de Investigação Médica 55 (LIM55), Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, SP, Brazil.
Gabriel Arantes Dos SantosLaboratorio de Investigação Médica 55 (LIM55), Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, SP, Brazil.
Iran SilvaLaboratorio de Investigação Médica 55 (LIM55), Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, SP, Brazil.
Katia Ramos Moreira LeiteLaboratorio de Investigação Médica 55 (LIM55), Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, SP, Brazil.
William NahasUro-Oncology Group, Urology Department, University of Sao Paulo Medical School and Institute of Cancer Estate of Sao Paulo (ICESP), Sao Paulo, Brazil.
Sabrina T ReisLaboratorio de Investigação Médica 55 (LIM55), Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, SP, Brazil.
Ruan PimentaLaboratorio de Investigação Médica 55 (LIM55), Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, SP, Brazil.
Nayara Izabel VianaLaboratorio de Investigação Médica 55 (LIM55), Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, SP, Brazil. niviana@usp.br.
Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo · BRUniversidade de São Paulo · BRAnhembi Morumbi University · BRTisch Hospital · USUniversidade do Estado de Minas Gerais · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bladder carcinoma (BC) is the tenth most frequent malignancy worldwide, with high morbidity and mortality rates. Despite recent treatment advances, high-grade BC and muscle-invasive BC present with significant progression and recurrence rates, urging the need for alternative treatments. The microRNA-21 (miR-21) has superexpression in many malignancies and is associated with cellular invasion and progression. One of its mechanisms of action is the regulation of RECK, a tumor suppressor gene responsible for inhibiting metalloproteinases, including MMP9. In a high-grade urothelial cancer cell line, we aimed to assess if miR-21 downregulation would promote RECK expression and decrease MMP9 expression. We also evaluated cellular migration and proliferation potential by inhibition of this pathway. In a T24 cell line, we inhibited miR-21 expression by transfection of a specific microRNA inhibitor (anti-miR-21). There were also control and scramble groups, the last with a negative microRNA transfected. After the procedure, we performed a genetic expression analysis of miR-21, RECK, and MMP9 through qPCR. Migration, proliferation, and protein expression were evaluated via wound healing assay, colony formation assay, flow cytometry, and immunofluorescence.After anti-miR-21 transfection, miR-21 expression decreased with RECK upregulation and MMP9 downregulation. The immunofluorescence assay showed a significant increase in RECK protein expression (p < 0.0001) and a decrease in MMP9 protein expression (p = 0.0101). The anti-miR-21 transfection significantly reduced cellular migration in the wound healing assay (p < 0.0001). Furthermore, in the colony formation assay, the anti-miR-21 group demonstrated reduced cellular proliferation (p = 0.0008), also revealed in the cell cycle analysis by flow cytometry (p = 0.0038). Our results corroborate the hypothesis that miR-21 is associated with BC cellular migration and proliferation, revealing its potential as a new effective treatment for this pathology.

Indexed as

Gene Expression Regulation, NeoplasticGPI-Linked ProteinsMicroRNAsUrinary Bladder NeoplasmsCell Line, TumorCell MovementCell ProliferationHumansMatrix Metalloproteinase 9GPI-Linked ProteinsMatrix Metalloproteinase 9MicroRNAsMIRN21 microRNA, humanMMP9 protein, humanRECK protein, humanBladder cancerDisease progressionsMetalloproteinasesMicroRNARECK

Identifiers

PMID38522065
OpenAlexW4393130828

What OpenQuestion holds

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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.