Journal
MOLECULAR MEDICINE REPORTS
Volume 14, Issue 5, Pages 4795-4801Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2016.5832
Keywords
microRNA-203; B-cell-specific Moloney murine leukemia virus insertion site-1; multiple myeloma
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Funding
- National Natural Science Foundation of China [81201872]
- Natural Science Foundation of Fujian Province [2011101308]
- Foundation of Fujian Key Laboratory of Hematology [200911004]
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The oncogene B-cell-specific Moloney murine leukemia virus insertion site-1 (Bmi-1) is overexpressed in multiple myeloma (MM). Our previous study demonstrated that Bmi-1 silencing sensitized MM cells to bortezomib. Translational regulation has emerged as a prominent underlying mechanism of Bmi-1 regulation, particularly via microRNA targeting. The present study determined that Bmi-1 may be directly targeted by miR-203 using a luciferase assay. In addition, enforced expression of miR-203 led to significant downregulation of Bmi-1 protein and mRNA expression levels. Furthermore, restoration of miR-203 significantly inhibited cell growth and G1/S transition in MM cells. miR-203 was downregulated in MM patients, and a negative correlation between the expression of miR-203 and Bmi-1 was observed. The results of the present study indicated that miR-203 exerts growth-inhibiting effects in MM through the suppression of Bmi-1 expression. In conclusion, the present study demonstrated that Bmi-1 is a direct functional target of miR-203 in MM.
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