The regulation of miR-320a/XBP1 axis through LINC00963 for endoplasmic reticulum stress and autophagy in diffuse large B-cell lymphoma

Abstract Background This study incorporates fundamental research referring to considerable amounts of gene-sequencing data and bioinformatics tools analyze the pathological mechanisms diffuse large B-cell lymphoma (DLBCL). Methods A lncRNA-miRNA-mRNA ceRNA network DLBCL was constructed through database analysis combining GTEx TCGA. qPCR used detect expression LINC00963 miR-320a in cell lines. After or overexpression vitro, western blot performed assess protein levels UPR sensors (GRP78, p-IRE1, IRE1, active ATF6, ATF4 XBP1), along with apoptosis markers (Bcl-2, Bax, caspase 3) autophagy indicators (Beclin1, LC3II, LC3I p62). Additionally, LC3 analyzed immunofluorescence (IF) assay. Results Following SUDHL4 line showed a marked increase level UPR-related GRP78, p-IRE1 spliced XBP-1/XBP-1(s), apoptosis-related Bax cleaved 3, as well autophagy-related Beclin1 whereas mimic greatly diminished effects overexpression. Moreover, targeted while bound 3’UTR XBP1. It also found that resulted significantly delayed tumor growth xenograft model DLBCL. Conclusion Mechanistically, LINC00963/miR-320a regulated XBP1-apoptosis pathway autophagy, implying therapeutic potential this for selective targeting. The presented here illustrated mechanism LINC00963/miR-320a/XBP1 first time.