MALAT1 long non-coding RNA is overexpressed in multiple myeloma and may serve as a marker to predict disease progression

Background: The pathogenesis of multiple myeloma involves complex genetic and epigenetic events. This study aimed to investigate the role and clinical relevance of the long non-coding RNA (lncRNA), metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in multiple myeloma. Methods: Bone marrow mononuclear cells were collected for analysis. The samples of multiple myeloma were taken from 45 patients at diagnosis, 61 post-treatment, and 18 who relapsed or had progression. Control samples were collected from 20 healthy individuals. Real-time quantitative reverse transcription polymerase chain reactions were performed to evaluate the expression of MALAT1. The clinical relevance of MALAT1 expression was also explored. Results: MALAT1 was overexpressed in the newly diagnosed patients compared with post-treatment patients (mean Delta C-T: -5.54 +/- 0.16 vs. -3.84 +/- 0.09, 3.25-fold change; p < 0.001) and healthy individuals (mean Delta CT: -5.54 +/- 0.16 vs. -3.95 +/- 0.21, 3.01-fold change; p < 0.001). The expression of MALAT1 strongly correlated with disease status, and the magnitude of change in MALAT1 post-treatment had prognostic relevance. The patients with early progression had a significantly smaller change in MALAT1 after treatment (mean Delta C-T change: 1.26 +/- 1.06 vs. 2.09 +/- 0.79, p = 0.011). A cut-off value of the change in MALAT1 (Delta C-T change: 1.5) was obtained, and the patients with a greater decrease in MALAT1 (difference in Delta C-T > 1.5) had significantly longer progression-free survival compared with the patients with a smaller MALAT1 change (24 months vs. 11 months; p = 0.001). For the post-treatment patients, the risk of early progression could be predicted using this cut-off value. Conclusions: MALAT1 was overexpressed in patients with myeloma and may play a role in its pathogenesis. In addition, MALAT1 may serve as a molecular predictor of early progression.