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.
Highlights
Multiple myeloma (MM) is a malignant plasmacell (PC) disorder and clinically defined when a PC neoplasm results in clinical complications [1]
Our findings suggested that metastasis associated lung adenocarcinoma transcript 1 (MALAT1)/miR-509-5p/Forkhead box P1 (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
The results revealed that MALAT1 expression was significantly upregulated in MM patients compared to normal healthy controls (Figure 1A; P
Summary
Multiple myeloma (MM) is a malignant plasmacell (PC) disorder and clinically defined when a PC neoplasm results in clinical complications [1]. The disease is characterized by clonal proliferation of malignant plasma cells in the bone marrow, monoclonal para protein in blood/urine, and related organ dysfunction [3]. Despite significant progress in elucidation of the biology and treatment options over the past few decades, myeloma remains incurable, and the five-year survival rate of MM is about 40% [4]. Increasing studies suggested that dysregulated expressions www.impactjournals.com/oncotarget of lncRNA occur in various diseases and might contribute to cancer biology [8]. Li et al showed that overexpression of lncRNA HOTTIP increased chemoresistance of osteosarcoma cells by activating the Wnt/β-catenin pathway [10]. Cui et al revealed that lncRNA SNHG1 contributed to the progression of nonsmall cell lung cancer through inhibition of miR-101-3p and activation of Wnt/β-catenin signaling pathway [11]. The functional role and underlying mechanism of MALAT1 in MM remains unclear
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