Abstract
INTRODUCTION: Emerging evidence has indicated that long non-coding RNAs (lncRNAs) play vital roles in multiple myeloma (MM) development and progression. However, the underlying mechanism of PVT1 in MM remains unclear. MATERIAL AND METHODS: QRT-PCR was used to detect the expression of PVT1 and miR-203a in MM samples and cell lines. The effects of PVT1 on MM cell proliferation and apoptosis were determined by CCK8 assay and flow cytometer assay, respectively. Bioinformatics methods were used to identify the downstream target miRNAs of PVT1. RESULTS: We found that the expression of PVT1 was upregulated in MM samples and cell lines (p < 0.05), while the expression of miR-203a was downregulated in MM samples and cell lines (p < 0.05). There was a negative correlation between PVT1 expression and miR-203a expression in MM samples (p < 0.05). In in vitro function assays, we found that PVT1 inhibition suppressed MM cell proliferation and induced MM cell apoptosis (p < 0.05). The bioinformatics approach predicted that PVT1 sponge miR-203a would modulate MM cells. Rescue experiments confirmed the recovering roles of miR-203a for PVT1 on MM progression. CONCLUSIONS: In the present study, we found that lncRNA PVT1 could promote MM cell proliferation and induce cell apoptosis by inhibiting miR-203a expression. Therefore, PVT1 may represent a potential therapeutic target for the treatment of MM patients.