BTG2 inhibits the proliferation and metastasis of osteosarcoma cells by suppressing the PI3K/AKT pathway

被引:2
|
作者
Li, Yi-Jin [1 ]
Dong, Bao-Kang [1 ]
Fan, Meng [1 ]
Jiang, Wen-Xue [1 ]
机构
[1] Tianjin First Cent Hosp, Dept Orthopaed Surg, Tianjin 300192, Peoples R China
来源
INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY | 2015年 / 8卷 / 10期
关键词
B cell translocation gene 2 (BTG2); osteosarcoma; proliferation; invasion; PI3K/AKT pathway; TUMOR PROGRESSION; DOWN-REGULATION; BREAST-CANCER; MIGRATION; INVASION; EXPRESSION; AKT; REGULATOR; PROGNOSIS; AKT/PKB;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
B cell translocation gene 2 (BTG2) has been reported to be a potential tumor suppressor in many types of tumors. However, the roles and molecular mechanisms of BTG2 in osteosarcoma progression are still unknown. In this study, we investigated the role of BTG2 in proliferation and metastasis of osteosarcoma and the underlying mechanism. BTG2 expression levels were measured in fresh osteosarcoma tissues and cell lines. The effects of BTG2 on cell proliferation, migration and invasion were explored by MTT, transwell assays, western blot, and in vivo tumorigenesis in nude mice. We found that BTG2 was down-regulated in human osteosarcoma tissues and cell lines. Overexpression of BTG2 inhibited the proliferation and migration/invasion of human osteosarcoma cells in vitro, it also markedly inhibited xenograft tumor growth in vivo. Furthermore, BTG2 significantly decreased the expression of phosphorylated PI3K and AKT in osteosarcoma cells. Taken together, our data indicate that BTG2 might suppress the tumor growth and metastasis via PI3K/AKT signaling pathway, implying that BTG2 may serve as a potential molecular target for the treatment of osteosarcoma.
引用
收藏
页码:12410 / 12418
页数:9
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