Abstract
Previous studies showed that Metastasis associated lung adenocarcinoma transcript 1(MALAT1) acted as an oncogene in Multiple Myeloma (MM). However, the underlying mechanism of MALAT1 in MM remains unclear. Quantitative real time-PCR(qRT-PCR) was used to determine MALAT1 expression in MM samples and cell lines. in vitro function assays were used to determine the function of MALAT1 on MM cells. Bioinformatics tools were used to predict the targets of MALAT1 and miR-509-5p, respectively. Furthermore, rescue experiments were performed to further confirm the regulation of miR-509-5p by MALAT1. In the present study, our data showed that MALAT1 expression was upregulated in MM samples and cell lines. In function assays, we confirmed that MALAT1 inhibition significantly suppressed cells proliferation, induced cells apoptosis, arrested cells in G1/S phase, and inhibited MM cells growth in vivo. Furthermore, MALAT1 was identified to function as a competitive endogenous RNA (ceRNA) for miR-509-5p to promote MM cell viability. Additionally, our results suggested that miR-509-5p targeted the 3'-UTR of FOXP1 to suppress MM cells progression. Meanwhile, our results showed that miR-509-5p inhibitors significantly abrogated the decreased expression of FOXP1 induced by MALAT1 suppression, indicating that MALAT1 could positively regulate FOXP1 expression by sponging miR-509-5p. Our findings suggested that MALAT1/miR-509-5p/FOXP1 axis was one of the key signalings in mediating MM cell growth, and further indicated that MALAT1 could act as a novel diagnostic marker and therapeutic target for the treatment of MM.