miR-103a-3p suppresses cell proliferation and migration in Hirschsprung’s disease partly by targeting PIK3R1

Abstract

AbstractObjective To elucidate the function and mechanism of the miR-103a-3p in the development of HSCR. Methods PCR was used to confirm the differential miR-103a-3p expression in tissue specimens. Then, CCK-8 and transwell assays were used to determine the effect of miR-103a-3p on cell proliferation and migration. MiRNA Target predict software Kyoto Encyclopedia of Genes Genomes (KEGG), Gene Ontology (GO) and protein–protein interaction network (PPI) analyses were used to predict possible target genes. Then, PCR, automated immunoblotting, dual luciferase reporter assays and rescue assays were used to confirm the target genePIK3R1 in vitroandin tissue. Results miR-103a-3p was significantly upregulated in HSCR colon tissues. miR-103a-3p inhibited cell growth and migrationin vitro.Bioinformatic analysis suggested thatPI3KR1was a potential target of miR-103a-3p in HSCR. miR-103a-3p can bind toPI3KR1and affectPI3KR1mRNA expression and protein levels. The negative correlation between miR-103a-3p andPI3KR1was confirmed in tissue samples. A rescue assay also demonstrated thatPI3KR1can partially reverse the effect of miR-103a-3p on cell proliferation and migration. Conclusions miR-103a-3p can inhibit cell growth and motility, partially by targetingPI3KR1. miR-103a-3p plays an important role in the development of HSCR.