Inhibition of Six1 promotes apoptosis, suppresses proliferation, and migration of osteosarcoma cells

骨肉瘤 细胞周期蛋白D1 细胞生长 细胞凋亡 癌症研究 细胞周期 细胞培养 流式细胞术 细胞迁移 细胞 化学 细胞生物学 生物 分子生物学 生物化学 遗传学
作者
Hua Liu,Liu Fan,Aichun Wei,Zhou Yongjin,Qingqing Chen,Wang Xiaojian
出处
期刊:Tumor Biology [SAGE Publishing]
卷期号:35 (3): 1925-1931 被引量:22
标识
DOI:10.1007/s13277-013-1258-1
摘要

Sineoculis homeobox homolog 1 (Six1) is one of the transcription factors that act as master regulators of development and is frequently dysregulated in cancers. However, the biological role of Six1 is not clear in osteosarcoma. To address the expression of Six1 in osteosarcoma cells, three osteosarcoma cell lines (U2OS, SaOS-2, and MG63) and a human osteoblastic cell line (hFOB1.19) were used to detect the expression of Six1 by quantitative real-time polymerase chain reaction and western blotting. The results showed that Six1 was upregulated in osteosarcoma cell lines compared to human osteoblastic cell line hFOB1.19. To investigate the role of Six1 in osteosarcoma cells, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, flow cytometry analysis, and transwell chamber assays were used to determine the effects of Six1 on the cell viability, cycle, apoptosis, and migration properties in U2OS cells. The results showed that Six1 could promote U2OS cell proliferation and migration, and suppress U2OS cell apoptosis. In addition, we investigated the effects of Six1 on the expression of following proteins (cyclin D1, caspase-3, and vascular endothelial growth factor-C (VEGF-C)). Results showed that Six1 could increase the expression of cyclin D1 and VEGF-C, and decrease the expression of caspase-3. All these data suggested that Six1 might be involved in the promotion of growth, proliferation, and migration of U2OS cells, as well as the inhibition of apoptosis of U2OS cells. These data might provide information for the prediction of osteosarcoma prognosis and potential targets for therapy of osteosarcoma.

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