Evidence map›Paper›PMID 42584802›Full record

ArticleMolecular biology reports2026

hnRNP A1 controls MIR17HG alternative splicing and maturation of miR-19a.

Vivian Maltese Munhoz, Letícia Oliveira Rojas Cruz, Patricia Pereira Coltri

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Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Vivian Maltese MunhozDepartamento de Biologia Celular e do Desenvolvimento, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, 05508-000, SP, Brazil.
Letícia Oliveira Rojas CruzDepartamento de Biologia Celular e do Desenvolvimento, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, 05508-000, SP, Brazil.
Patricia Pereira ColtriDepartamento de Biologia Celular e do Desenvolvimento, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, 05508-000, SP, Brazil. coltri@usp.br.ORCID https://orcid.org/0000-0001-8447-7516

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlternative splicing is a key process in the regulation of gene expression in eukaryotes. During transcription, the spliceosome machinery assembles onto precursor messenger RNA (pre-mRNA) conserved regions, promoting intron removal and exon ligation. This process is guided and controlled by the association of RNA-binding proteins (RBPs) in the pre-mRNAs. These proteins mediate splice-site choice controlling the splicing profile observed in different cells. The heterogeneous ribonucleoproteins (hnRNPs) A1 and K have previously been associated with intronic regions containing microRNAs (miRNAs). We previously showed hnRNP A1 overexpression increases invasion and cell growth in thyroid carcinoma cells through association with miR-17a and miR-18a. MIR17HG is the host gene for the miR-17-92 miRNA cluster, which is encoded within one of its introns. In this work, we investigated the participation of hnRNP A1 and hnRNP K in MIR17HG alternative splicing. METHODS AND

resultsOverexpression of hnRNP A1 and hnRNP K was performed using pFLAG system in HEK-293FT cells. Reverse transcription quantitative PCR (RT-qPCR) analysis indicated higher levels of MIR17HG-i3 isoforms, which correlated with increase on pre-miR-19a generation upon hnRNP A1 overexpression. Surprisingly, the same pattern was not observed in cells overexpressing hnRNP K. Higher concentration of functional miR-19a in hnRNP A1 overexpressing cells was confirmed by luciferase reporter assays.

conclusionsThese results indicate that hnRNP A1 modulates MIR17HG splicing, with downstream effects on miR-19a biogenesis and maturation.

Indexed as

Alternative SplicingHeterogeneous Nuclear Ribonucleoprotein A1MicroRNAsHEK293 CellsHeterogeneous-Nuclear Ribonucleoprotein KHumansIntronsRNA PrecursorsHeterogeneous Nuclear Ribonucleoprotein A1Heterogeneous-Nuclear Ribonucleoprotein KhnRNPA1 protein, humanMicroRNAsMIR17, humanMIR19A, humanRNA PrecursorsAlternative splicingmiR-17-92MIR17HGmiR-19aRBP

Identifiers

PMID42584802
PMCPMC13468856

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