The interaction of hepatoma-derived growth factor and beta-catenin promotes tumorigenesis of synovial sarcoma
The interaction of hepatoma-derived growth factor and beta-catenin promotes tumorigenesis of synovial sarcoma
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肝癌源性生长因子与β-catenin的相互作用促进滑膜肉瘤的发生
DOI：
10.1007/s13277-016-4905-5
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发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Han Anjia
中科院分区：
文献类型：
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作者：
Tang Jianming;Shi Huijuan;Li Hui;Zhen Tiantian;Dong Yu;Zhang Fenfen;Yang Yang;Han Anjia
目的探讨肝肿瘤源性生长因子（HDGF）和β-连环蛋白在滑膜肉瘤中的临床病理和生物学作用。我们的研究结果表明，组织学类型和HDGF/β-catenin表达是滑膜肉瘤患者总生存的两个重要独立预后因素。HDGF敲低显著抑制SW982细胞的增殖、集落形成和迁移，但诱导G1期阻滞和凋亡。重组HDGF增强了滑膜肉瘤细胞的生长，部分恢复了敲除HDGF后SW982细胞的生长抑制。HDGF敲低显著抑制SW982细胞中β-catenin及其下游基因的表达。有趣的是，β-catenin敲低显著抑制SW982细胞中HDGF的表达。在SW982细胞中发现了HDGF和β-catenin的直接相互作用。在SW982细胞中发现了β-catenin启动子中的3个hdgf结合元件，这些元件对β-catenin的转录激活具有特异性。总之，我们的研究结果首先表明HDGF和β-catenin的相互作用可能在滑膜肉瘤的肿瘤发生中起关键作用。
To clarify the clinicopathological and biological role of hepatoma-derived growth factor (HDGF) and β-catenin in synovial sarcoma. Our results showed that histological type and HDGF/β-catenin expression were the two important independent prognostic factors for overall survival in synovial sarcoma patients. HDGF knockdown dramatically inhibited cellular proliferation, colony formation, and migration but induced G1 phase arrest and apoptosis in SW982 cells. Recombinant HDGF enhanced synovial sarcoma cell growth and partially retrieved the cell growth suppression in SW982 cells upon HDGF knockdown. HDGF knockdown dramatically suppressed β-catenin and its downstream gene expression in SW982 cells. Intriguingly, β-catenin knockdown dramatically suppressed HDGF expression in SW982 cells. A direct interaction of HDGF and β-catenin was found in SW982 cells. Three HDGF-binding elements in β-catenin promoter were found and specific for transcriptional activation of β-catenin in SW982 cells. In conclusion, our findings first indicate that the interaction of HDGF and β-catenin may play a crucial role in tumorigenesis of synovial sarcoma.