Sulian Chen, Lihua Zhu, Jing Huang, Ying Cai, Xiaohui Lu, Qingling Yang, Qiong Wu, Changjie Chen and Zhiwei Wang Pages 5354 - 5361 ( 8 )
Background: Arsenic trioxide (As<sub>2</sub>O<sub>3</sub>) has been demonstrated to suppress tumorigenesis in human glioma. However, the exact molecular mechanisms by which As<sub>2</sub>O<sub>3</sub> exerts its tumor suppressor functions are elusive. Therefore, it is warranted to explore the underlying mechanism of As<sub>2</sub>O<sub>3</sub>–mediated anti-tumor activity in glioma. </p> <p> Methods: To achieve our goal, we used multiple approaches including MTT assay, apoptosis, Real-time RT-PCR, Western blotting, invasion assay, and gene transfection. </p> <p> Results: We observed that A<sub>2</sub>2O<sub>3</sub> inhibited cell growth and induced apoptosis as well as suppressed migration and invasion in human glioma cells. Moreover, we found that As<sub>2</sub>O<sub>3</sub> down-regulated miR-125b expression and subsequently up-regulated its target gene Bak1 expression. Furthermore, we identified that As<sub>2</sub>O<sub>3</sub> exerts its anti-tumor activity partly through regulation of miR-125b. </p> <p> Conclusions: Our present study suggests that As<sub>2</sub>O<sub>3</sub> could be a potential therapeutic agent for treatment of human glioma.
As<sub>2</sub>O<sub>3</sub>, glioma, invasion, miR-125b, Bak1.
, , , , , , , , Department of Biochemistry and Molecular Biology, Bengbu Medical College, Anhui 233030, China.