中国组织工程研究

中国组织工程研究 ›› 2012, Vol. 16 ›› Issue (32): 5988-5992.doi: 10.3969/j.issn.2095-4344.2012.32.019

• 肿瘤干细胞 cancer stem cells • 上一篇    下一篇

细胞信号负调控因子3调控Wnt/β-Catenin信号通路对肿瘤干细胞的影响及其在脑胶质母细胞瘤中的应用

吴 伟   

  1. 成都市第一人民医院神经外科，四川省成都市 610041
  • 收稿日期:2012-05-12 修回日期:2012-06-11 出版日期:2012-08-05 发布日期:2012-08-05
  • 作者简介:吴伟，男，1976年生，四川省成都市人，汉族，1999年华西医科大学毕业，主治医师，主要从事神经外科方面的研究。 weijunhr008@sina.com

Effect of Wnt/β-Catenin signal pathway adjusted by suppressor of cytokine signaling 3 on tumor stem cells and its application in treatment of glioblastoma multiforme

Wu Wei   

  1. Department of Neurosurgery, First People’s Hospital of Chengdu, Chengdu 610041, Sichuan Province, China
  • Received:2012-05-12 Revised:2012-06-11 Online:2012-08-05 Published:2012-08-05
  • About author:Wu Wei, Attending physician, Department of Neurosurgery, First People’s Hospital of Chengdu, Chengdu 610041, Sichuan Province, China weijunhr008@sina.com

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摘要：

背景：有研究表明，细胞信号负调控因子3、Wnt/β-Catenin信号通路与脑胶质母细胞瘤的发生密切相关。
目的：探讨细胞信号负调控因子3与Wnt/β-Catenin信号通路对肿瘤干细胞的影响及在治疗脑胶质母细胞瘤中的作用机制。
方法：从手术切除的脑胶质母细胞瘤标本中，分离、培养及鉴定脑肿瘤干细胞。反转录PCR扩增细胞信号负调控因子3基因，转染至脑胶质母细胞瘤干细胞。反转录PCR、Western blot检测细胞信号负调控因子3转染前后，脑胶质母细胞瘤干细胞中细胞信号负调控因子3、信号转导与转录活化因子3、β-Catenin及抑癌因子人第10号染色体缺失磷酸酶及张力蛋白同源基因mRNA及蛋白的表达。
结果与结论：高表达细胞信号负调控因子3可能通过抑制信号转导与转录活化因子3的表达，从而抑制Wnt/β-Catenin通路的传导，以增强人第10号染色体缺失磷酸酶及张力蛋白同源基因活性，降低胶质瘤细胞增殖及侵袭能力同时诱导细胞凋亡，为脑胶质母细胞瘤的靶向治疗提供新的途径。

关键词: 细胞信号负调控因子3, Wnt/β-Catenin信号通路, 脑胶质母细胞瘤, 信号转导与转录活化因子3, 人第10号染色体缺失磷酸酶及张力蛋白同源基因

Abstract:

BACKGROUND: Several studies have demonstrated that suppressor of cytokine signaling 3 (SOCS3) and Wnt/β-Catenin signal pathway are associated with the occurrence of glioblastoma multiforme.
OBJECTIVE: To investigate the effect of Wnt/β-Catenin adjusted by SOCS3 on tumor stem cells and its application in treatment of glioblastoma multiforme.
METHODS: GBM stem cells were isolated from resected glioblastoma multiforme tissues. Then they were also cultured and identified. SOCS3 was amplified by RT-PCR and transfected to glioblastoma multiforme stem cells. RT-PCR and western blotting were employed to determine the mRNA and protein expression of SOCS3, signal transducer and activator of transcription 3 (STAT3), β-Catenin and phosphatase and tensin homology deleted on chromosome ten (PTEN) before and after transfection.
RESULTS AND CONCLUSION: After SOCS3 transfection, the expression of SOCS3 increased, thus the expression of STAT3 and β-Catenin decreased significantly (P < 0.05). However, Wnt/β-Catenin signal pathway was inhibited. The activity of PTEN was increased significantly (P < 0.05). High expression of SOCS3 can inhibit the conduction of Wnt/β-Catenin signal pathway by decreasing the expression of STAT3. It can also enhance the activity of PTEN, and decrease the proliferation and invasion ability of glioma cells significantly while inducing apoptosis. It offers a new way for target therapy of glioblastoma multiforme.

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