.png){kind=icon}
.png){kind=icon}
Return
hnRNP A1 controls MIR17HG alternative splicing and maturation of miR-19a
.png){kind=icon}
OA
AI
V
L
P
DOI：10.1007/s11033-026-12580-6.png)
.png){kind=icon}
.png){kind=icon}
Share.png){kind=icon}
Save
Abstract
En 中文
Alternative 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. Overexpression 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. These results indicate that hnRNP A1 modulates MIR17HG splicing, with downstream effects on miR-19a biogenesis and maturation.
Keywords:
RBP
MIR17HG
miR-19a
miR-17-92
Alternative splicing
AI Summary
Key information extracted from the uploaded paper, including a brief overview, abstract, background, key highlights, visual analysis, and future outlook.
Journal
IF:
2.8
Papers:
2.2K
Citations:
1.9W
Organization
Cited Papers