Abstract

Abstract Objective: We aimed to study the effect of triptolide on OS and the related molecular mechanism. Methods: The cell viability, apoptosis portion, tumor size, tumor weight and invasion of OS cells were determined. The relative level of miR-181 in OS tissues and the adjacent tissues was determined by qRT-PCR. The target gene of miR-181a was determined and verified by luciferase report assay. At last, OS cells were treated with triptolide and triptolide + miR-181a mimics to verify the relationship between triptolide and miRN-181a. Results: Triptolide inhibited the cell viability, promoted the apoptosis, decreased the tumor size and weight, and reduced the invasion of OS cells. The level of miR-181a in OS cells decreased significantly after treating with triptolide, and the relative level of miR-181a in OS tissues was markedly higher than that in the adjacent tissues. PTEN was reported and verified the direct target gene of miR-181a. The overexpression of miR-181a decreased the inhibition of triptolide on OS proliferation and promotion on OS apoptosis. Conclusion: Triptolide inhibited the proliferation of OS by regulating miR-181a via targeting PTEN gene in vivo and vitro. Note: This abstract was not presented at the meeting. Citation Format: Chunming Jiang, Xiang Fang, Xuepeng Wang, Maoqiang Li, Wu Jiang, Liulong Zhu, Zhenyu Bian. Triptolide inhibits the growth of osteosarcoma by regulating microRNA-181a via targeting PTEN gene in vivo and in vitro [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 1482. doi:10.1158/1538-7445.AM2017-1482

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