Lncrna St3gal6-As1 Promotes Invasion By Inhibiting Hnrnpa2b1-Mediated St3gal6 Expression In Multiple Myeloma

Multiple myeloma (MM) is an incurable disease caused by the infiltration of malignant plasma B cells into bone marrow, whose pathogenesis remains largely unknown. Long non-coding RNAs (lncRNAs) have emerged as important factors in pathogenesis. Our previous study validated that lncRNA ST3 beta-galactoside alpha-2,3-sialyltransferase 6 antisense RNA 1 (ST3GAL6-AS1) was upregulated markedly in MM. Therefore, the aim of the study was to investigate the molecular mechanisms of ST3GAL6-AS1 in MM cells. ST3GAL6-AS1 expression levels in MM cells was detected using reverse transcription-quantitative PCR. ST3GAL6-AS1 antisense oligonucleotides and small interfering RNAs were transfected into MM cells to downregulate expression. In vitro assays were performed to investigate the functional role of ST3GAL6-AS1 in MM cells. RNA pull-down, RNA immunoprecipitation and comprehensive identification of RNA-binding proteins using mass spectrometry assays were used to determine the mechanism of ST3GAL6-AS1-mediated regulation of underlying targets. It was reported that knockdown of ST3GAL6-AS1 suppressed the adhesion, migration and invasion ability of MM cells in vitro. Expression of ST3GAL6 was significantly reduced when ST3GAL6-AS1 was knock downed in MM cells. Moreover, mechanistic investigation showed that ST3GAL6-AS1 could suppress ST3GAL6 mRNA degradation via interacting with heterogeneous nuclear ribonucleoprotein A2B1 (hnRNPA2B1). The present results suggested that upregulated lncRNA ST3GAL6-AS1 promotes adhesion and invasion of MM cells by binding with hnRNPA2B1 to regulate ST3GAL6 expression.