| Literature DB >> 25971527 |
Xianjuan Shen1, Yuehua Guo2, Jiajia Yu3, Jing Qi1, Wei Shi1, Xinhua Wu1, Hongbing Ni4, Shaoqing Ju5,6,7.
Abstract
Bone marrow stromal cells (BMSCs) up-regulate B cell-activating factor (BAFF) in multiple myeloma. Increasing experimental evidence has shown that microRNAs play a causal role in hematology tumorigenesis. In this study, we characterized the role of miR-202 in regulating the expression of BAFF in BMSCs. It was found that expressions of BAFF mRNA and protein were increased in BMSCs treated with miR-202 inhibitor. The growth rate of miR-202 mimics transfection cells was significantly lower than that of non-transfected cells. The expression of Bcl-2 protein was down-regulated, and Bax protein was up-regulated after miR-202 mimics transfection. Over-expression of miR-202 in BMSCs rendered MM cells more sensitive to bortezomib. More significantly, the regulatory effect of miR-202 could inhibit the activation of NF-κB pathway in BMSCs. These results suggest that miR-202 functions as a modulator that can negatively regulate BAFF by inhibiting MM cell survival, growth, and adhesion in the bone marrow microenvironment.Entities:
Keywords: B cell-activating factor (BAFF); Bone marrow stromal cells (BMSCs); Drug resistance; Multiple myeloma (MM); microRNA-202 (miR-202)
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Year: 2015 PMID： 25971527 DOI： 10.1007/s10238-015-0355-4
Source DB: PubMed Journal: Clin Exp Med ISSN： 1591-8890 Impact factor: 3.984