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Published on: December 31, 2014
miR-19a-3p Functions as an Oncogene by Regulating FBXO32 Expression in Multiple Myeloma
Ying Li1, Song Gao1, Wenjing Xue1
1Department of Hematology, Jinshan Hospital of Fudan University, Jinshan, Shanghai, PR China.
Background:
Multiple myeloma remains a virtually incurable hematologic malignancy, which is featured with the aberrant growth of malignant plasma cells.
Aims:
To elucidate the functions of miR-19a-3p in multiple myeloma.
Study Design:
Cell study.
Methods:
Cell counting kit-8 assay was performed to detect cell viability, and flow cytometry was conducted to detect cell apoptosis. Bioinformatics analysis predicted miR-19a-3p-associated biological function, pathway, core regulatory network, and target genes. Luciferase reporter assay verified the target sequence of miR-19a-3p regulating FBXO32.
Results:
miR-19a-3p is upregulated in multiple myeloma cells (p<0.01) and patients with multiple myeloma (p<0.001). Overexpressed miR-19a-3p significantly increased cell viability (p<0.05) and inhibited cell apoptosis (p<0.01). FBXO32 is a target gene of miR-19a-3p (p<0.01). Moreover, FBXO32 is downregulated in MM, and it significantly decreased cell viability (p<0.05) and promoted cell apoptosis (p<0.01). FBXO32 significantly rescued the influence of miR-19a-3p-inhibiting cell apoptosis (p<0.05).
Conclusion:
miR-19a-3p promoted cell proliferation and inhibited cell apoptosis by degrading the target FBXO32 mRNA in multiple myeloma.
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