miR-125 b expression affects tumor growth of multiple myeloma via targeting MKK 7
miR-125 b expression affects tumor growth of multiple myeloma via targeting MKK 7
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发表时间：
2017
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通讯作者：
Yanxia Jiang;Yajing Luan;D. He;Guoan Chen
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作者：
Yanxia Jiang;Yajing Luan;D. He;Guoan Chen
据报道，许多miRNA参与肿瘤的发展。miRNAs驱动多发性骨髓瘤（MM）进展的潜在机制仍然难以捉摸。本研究旨在探讨miR-125 b对丝裂原活化蛋白激酶7（mitogen-activated protein kinase 7，MKK 7）的影响。我们发现MM中miR-125 b的显著上调和MKK 7的失调。在多发性骨髓瘤样品和细胞系中进一步证实了负相关。此外，MKK 7被鉴定为miR-125 b的下游靶基因，其可以结合MKK 7的3' UTR。miR-125 b的过表达与MKK 7的表达降低相关，miR-125 b拮抗剂可抑制细胞增殖和克隆形成。综上所述，我们的研究结果表明，MKK 7可以作为一个重要的肿瘤抑制剂在MM中被miR-125 b中和，这表明miR-125 b可能是一个新的潜在的分子治疗靶点在MM的治疗。
Many miRNAs are reported to be involved in tumor development. The underlying mechanism of miRNAs driving multiple myeloma (MM) progress remains elusive. This study is to investigate the effect of miR-125b, a brainenriched microRNA, on mitogen-activated protein kinase 7 (MKK7) in vivo. We found significantly up-regulation of miR-125b and deregulation of MKK7 in MM. The inverse correlation was further confirmed in multiple myeloma samples and cell lines. In addition, MKK7 was identified as a downstream target gene of miR-125b, which could bind to the 3’ UTR of MKK7. Overexpression of miR-125b was associated with decreased MKK7 expression and miR-125b antagonisminhibited cell proliferation and clonogenicity. Taken together, our results demonstrated that MKK7 could function as an important tumor suppressor neutralized by miR-125b in MM, suggesting that miR-125b may be a novel potential molecular therapeutic target in the treatment of MM.