Chinese Journal of Tissue Engineering Research ›› 2012, Vol. 16 ›› Issue (32): 5988-5992.doi: 10.3969/j.issn.2095-4344.2012.32.019

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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

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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