lncRNA ST3GAL6­AS1 promotes invasion by inhibiting hnRNPA2B1­mediated 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 non­coding RNAs (lncRNAs) have emerged as important factors in pathogenesis. Our previous study validated that lncRNA ST3 ß­galactoside α­2,3­sialyltransferase 6 antisense RNA 1 (ST3GAL6­AS1) was upregulated markedly in MM. Therefore, the aim of the study was to investigate the molecular mechanisms of ST3GAL6­AS1 in MM cells. ST3GAL6­AS1 expression levels in MM cells was detected using reverse transcription­quantitative PCR. ST3GAL6­AS1 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 ST3GAL6­AS1 in MM cells. RNA pull­down, RNA immunoprecipitation and comprehensive identification of RNA­binding proteins using mass spectrometry assays were used to determine the mechanism of ST3GAL6­AS1­mediated regulation of underlying targets. It was reported that knockdown of ST3GAL6­AS1 suppressed the adhesion, migration and invasion ability of MM cells in vitro. Expression of ST3GAL6 was significantly reduced when ST3GAL6­AS1 was knock downed in MM cells. Moreover, mechanistic investigation showed that ST3GAL6­AS1 could suppress ST3GAL6 mRNA degradation via interacting with heterogeneous nuclear ribonucleoprotein A2B1 (hnRNPA2B1). The present results suggested that upregulated lncRNA ST3GAL6­AS1 promotes adhesion and invasion of MM cells by binding with hnRNPA2B1 to regulate ST3GAL6 expression.