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 β‑galactoside α‑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.
Keywords: multiple myeloma; ST3GAL1-AS1; adhesion; invasion; heterogeneous nuclear ribonucleoprotein A2B1; ST3GAL6.