Abstract
Background: miR-429-mediated progression of multiple myeloma (MM) was studied through mediating B cell-specific Moloney murine leukemia virus integration site 1 (Bmi1)/protein kinase B (AKT) pathway. Methods: miRNA or siRNA was delivered into MM cell lines to alter cellular proliferation, apoptosis, invasion and migration. Measurements of miR-429 and Bmi1 levels were performed. AKT and p-AKT expression change was measured after regulating miR-429. The interaction between miR-429 and Bmi1 was analyzed. Results: miR-429 elevation disrupted proliferation, anti-apoptosis, migration and invasion properties of MM cells, and inactivated AKT pathway. Bmi1 was a targeting partner of miR-429, which was highly expressed in MM. Bmi1 knockdown phenotyped the effects of overexpressed miR-429 on MM cells. AKT agonist SC70 reversed miR-429-regulated inhibition of MM cell growth. Conclusion: miR-429 suppresses the activation of Bmi1/AKT pathway to down-regulate the malignant functions of MM cells.
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