Arsenic Trioxide Targets miR-125b in Glioma Cells

被引:15
作者
Chen, Sulian [1 ]
Zhu, Lihua [2 ]
Huang, Jing [2 ]
Cai, Ying [2 ]
Lu, Xiaohui [2 ]
Yang, Qingling [1 ]
Wu, Qiong [3 ]
Chen, Changjie [1 ]
Wang, Zhiwei [4 ]
机构
[1] Bengbu Med Coll, Dept Biochem & Mol Biol, Bengbu 233030, Anhui, Peoples R China
[2] Bengbu Med Coll, Clin Testing & Diagnose Expt Ctr, Bengbu 233000, Anhui, Peoples R China
[3] Bengbu Med Coll, Affiliated Hosp 1, Dept Med Oncol, Bengbu 233000, Anhui, Peoples R China
[4] Soochow Univ, Affiliated Hosp 1, Jiangsu Inst Hematol, Cyrus Tang Hematol Ctr, Suzhou 215123, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
As2O3; glioma; invasion; miR-125b; Bak1; PANCREATIC-CANCER CELLS; UP-REGULATION; INDUCED APOPTOSIS; EXPRESSION; GLIOBLASTOMA; LINE; THERAPY; GROWTH; RESISTANCE; PATHWAY;
D O I
10.2174/1381612820666140128204132
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Background: Arsenic trioxide (As2O3) has been demonstrated to suppress tumorigenesis in human glioma. However, the exact molecular mechanisms by which As2O3 exerts its tumor suppressor functions are elusive. Therefore, it is warranted to explore the underlying mechanism of As2O3-mediated anti-tumor activity in glioma. Methods: To achieve our goal, we used multiple approaches including MTT assay, apoptosis, Real-time RT-PCR, Western blotting, invasion assay, and gene transfection. Results: We observed that As2O3 inhibited cell growth and induced apoptosis as well as suppressed migration and invasion in human glioma cells. Moreover, we found that As2O3 down-regulated miR-125b expression and subsequently up-regulated its target gene Bak1 expression. Furthermore, we identified that As2O3 exerts its anti-tumor activity partly through regulation of miR-125b. Conclusions: Our present study suggests that As2O3 could be a potential therapeutic agent for treatment of human glioma.
引用
收藏
页码:5354 / 5361
页数:8
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