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 3â??-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.