Evidence map›Paper›PMID 37460706›Full record

ArticleHuman cell2023

Musashi-1 regulates cell cycle and confers resistance to cisplatin treatment in Group 3/4 medulloblastomas cells.

Pablo Shimaoka Chagas, Luciana Chain Veronez, Graziella Ribeiro de Sousa, Gustavo Alencastro Veiga Cruzeiro, Carolina Alves Pereira Corrêa, Fabiano Pinto Saggioro, Rosane Gomes de Paula Queiroz, Suely Kazue Nagahashi Marie, Silvia Regina Brandalise, Izilda Aparecida Cardinalli and 7 more

Abstract read
PubMed Publisher
In one paragraph

Article in Human cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

0 citing papers in PubMed, 3 citations in OpenAlex.

No citing paper in PubMed yet.

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

17 authors at 4 institutions in 2 countries.

Pablo Shimaoka Chagas *Department of Genetics, Ribeirão Preto Medical School-University of São Paulo, Bandeirantes Avenue, 3900, Ribeirão Preto, São Paulo, 14048-900, Brazil. pablochagas@usp.br.ORCID http://orcid.org/0000-0002-0652-728X
Luciana Chain Veronez *Department of Pediatrics, Clinics Hospital-Ribeirão Preto Medical School-University of São Paulo, Ribeirão Preto, Brazil.
Graziella Ribeiro de SousaDepartment of Genetics, Ribeirão Preto Medical School-University of São Paulo, Bandeirantes Avenue, 3900, Ribeirão Preto, São Paulo, 14048-900, Brazil.
Gustavo Alencastro Veiga CruzeiroDepartment of Pediatrics, Clinics Hospital-Ribeirão Preto Medical School-University of São Paulo, Ribeirão Preto, Brazil.
Carolina Alves Pereira CorrêaDepartment of Pediatrics, Clinics Hospital-Ribeirão Preto Medical School-University of São Paulo, Ribeirão Preto, Brazil.
Fabiano Pinto SaggioroDepartment of Pathology, Ribeirão Preto Medical School, 3900 Bandeirantes Avenue, Ribeirão Preto, SP, 14049-900, Brazil.
Rosane Gomes de Paula QueirozDepartment of Pediatrics, Clinics Hospital-Ribeirão Preto Medical School-University of São Paulo, Ribeirão Preto, Brazil.
Suely Kazue Nagahashi MarieLaboratory of Cellular and Molecular Biology, Department of Neurology, Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, SP, Brazil.
Silvia Regina BrandaliseBoldrini's Children Center, Campinas, SP, Brazil.
Izilda Aparecida CardinalliBoldrini's Children Center, Campinas, SP, Brazil.
José Andres YunesBoldrini's Children Center, Campinas, SP, Brazil.
Carlos Gilberto Carlotti JúniorDepartment of Surgery and Anatomy, Faculty of Medicine of Ribeirão Preto, University of Sao Paulo, São Paulo, Brazil.
Hélio Rubens MachadoDivision of Pediatric Neurosurgery, Department of Surgery and Anatomy, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.
Marcelo Volpon SantosDepartment of Surgery and Anatomy, Ribeirão Preto Medical School, University of São Paulo, Bandeirantes Av., Ribeirão Preto, SP, 390014049-900, Brazil.
Carlos Alberto ScrideliDepartment of Genetics, Ribeirão Preto Medical School-University of São Paulo, Bandeirantes Avenue, 3900, Ribeirão Preto, São Paulo, 14048-900, Brazil.
Luiz Gonzaga ToneDepartment of Genetics, Ribeirão Preto Medical School-University of São Paulo, Bandeirantes Avenue, 3900, Ribeirão Preto, São Paulo, 14048-900, Brazil.
Elvis Terci ValeraDepartment of Pediatrics, Clinics Hospital-Ribeirão Preto Medical School-University of São Paulo, Ribeirão Preto, Brazil.
Universidade de São Paulo · BRCentro Infantil Boldrini · BRBroad Institute · USClinics Hospital of Ribeirão Preto · BR

Funding

Fundação de Amparo à Pesquisa do Estado de São Paulo 2017/26160-5
6 · The paper itself

Abstract

Groups (Grp) 3 and 4 are aggressive molecular subgroups of medulloblastoma (MB), with high rates of leptomeningeal dissemination. To date, there is still a paucity of biomarkers for these subtypes of MBs. In this study, we investigated the clinical significance and biological functions of Musashi-1 (MSI1) in Grp3 and Grp4-MBs. First, we assessed the expression profile of MSI1 in 59 primary MB samples (15-WNT, 18-SHH, 9-Grp3, and 17-Grp4 subgroups) by qRT-PCR. MSI1 mRNA expression levels were also validated in an additional public dataset of MBs (GSE85217). The ROC curve was used to validate the diagnostic standards of MSI1 expression. Next, the potential correlated cell-cycle genes were measured by RNA-Seq. Cell cycle, cell viability, and apoptosis were evaluated in a Grp3/Grp4 MB cell line after knockdown of MSI1 and cisplatin treatment. We identified an overexpression of MSI1 with a high accuracy to discriminate Grp3/Grp4-MBs from non-Grp3/Grp4-MBs. We identified that MSI1 knockdown not only triggered transcriptional changes in the cell-cycle pathway, but also affected G2/M phase in vitro, supporting the role of knockdown of MSI1 in cell-cycle arrest. Finally, MSI1 knockdown decreased cell viability and sensitized D283-Med cells to cisplatin treatment by enhancing cell apoptosis. Based on these findings, we suggest that MSI1 modulates cell-cycle progression and may play a role as biomarker for Grp3/Grp4-MBs. In addition, MSI1 knockdown combined with cisplatin may offer a potential strategy to be further explored in Grp3/Grp4-MBs.

Indexed as

Antineoplastic AgentsCell CycleCerebellar NeoplasmsCisplatinDrug Resistance, NeoplasmMedulloblastomaNerve Tissue ProteinsRNA-Binding ProteinsApoptosisCell Line, TumorHumansAntineoplastic AgentsCisplatinMSI1 protein, humanNerve Tissue ProteinsRNA-Binding ProteinsGrp3-MBGrp4-MBsMedulloblastomaMusashi-1RNA-binding protein

Identifiers

PMID37460706
OpenAlexW4384522135

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.