Molecular Mechanism of Long Noncoding RNA B3GALT5-AS1 Targets miR-361-3p in Regulatng Proliferation and Apoptosis of Rat Pancreatic Scinar Cells

This study was aimed to investigate the regulation mechanism of lncRNA (long noncoding RNA) B3GALT5-AS1 (1,3-galactosyltransferase-polypeptide 5 antisense RNA) on the proliferation and apoptosis of rat pancreatic acinar cells induced by caerulein. AR42J cells were induced by caerulein to construct a model of acute pancreatitis cell injury; AR42J cells were transfected pcDNA-B3GALT5-AS1 group (transfected pcDNAB3GALT5-AS1), si-B3GALT5-AS1 group (transfected si-B3GALT5-AS1), miR-361-3p group (transfected miR361-3p mimics), anti-miR-361-3p group (transfected anti-miR-361-3p), pcDNA-B3GALT5-AS1+miR-361-3p group (co-transfected pcDNA-B3GALT5-AS1 and miR-361-3p mimics), si-B3GALT5-AS1+anti-miR-361-3p group (co-transfected si-B3GALT5-AS1 and anti-miR-361-3p) with lipidosome, and then induced by cellulin. CCK-8 (cell counting kit-8), flow cytometry, ELISA (enzyme-linked immunosorbent assay) seperately were used to detect cell proliferation rate, apoptosis rate, TNF-α (tumor necrosis factor-α) and IL-6 (interleukin-6) contents;  Western blot and qRT-PCR (real-time fluorescent quantitative reverse transcription polymerase chain reaction) were used to detect cyclin D1, survivin, procaspase-3 (precursor cysteine expression of acid aspartic protease-3), procaspase-9 (precursor cysteine aspartic protease-9) protein levels and B3GALT5-AS1, miR-361-3p expression; dual luciferase reporting experiment was used to detect the binding ability of B3GALT5-AS1 to miR-361-3p. Compared with the control group, the proliferation rate was significantly decreased; the apoptosis rate was significantly increased; the levels of TNF-α and IL-6 were significantly increased in AR42J cells induced by caerulein (P<0.05). B3GALT5-AS1 expression was abnormally reduced and miR-361-3p expression was abnormally increased in model cells. B3GALT5-AS1 overexpression or miR-361-3p inhibition could promote the proliferation; inhibit apoptosis, and up-regulate cyclin D1 and survivin. Procaspase-3, procaspase-9, inhibition of B3GALT5-AS1 and overexpression of miR-361-3p could inhibit the proliferation of damaged cells; promote cell apoptosis, and down-regulate the protein expression levels of cyclin D1, survivin, procaspase-3, and procaspase-9. B3GALT5-AS1 was capable of binding miR-361-3p. miR-361-3p could reverse the regulation of B3GALT5-AS1 on the proliferation and apoptosis of injured cells. lncRNA B3GALT5-AS1 could promote the proliferation and inhibit apoptosis of AR42J cells induced by caerulein, and the mechanism was related to targeting miR-361-3p.