Influence of 17-AAG on invasion and migration of colon cancer cells

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• 英文论文题名：Influence of 17-AAG on invasion and migration of colon cancer cells
• 论文作者：Zhao Xuerong ; Xiao Lijun ; Wang Jianping ; Chang Xiaomin
• 英文论文作者：Zhao Xuerong ; Xiao Lijun ; Wang Jianping ; Chang Xiaomin ; Department of immunology ; Chengde Medical University
• 年：2016
• 作者机构：Department of immunology,Chengde Medical University;
• 英文论文关键词：17-AAG ; HCT-15 ; HCT-116 ; invasion ; migration
• 会议召开时间：2016-11-04
• 会议录名称：第十一届全国免疫学学术大会摘要汇编
• 英文会议录名称：Abstracts of 2016 CSI Congress on Immunology
• 语种：英文
• 分类号：R735.34
• 学会代码：IGMD
• 会议名称：第十一届全国免疫学学术大会
• 会议地点：中国安徽合肥
• 主办单位：中国免疫学会
• 学会名称：中国免疫学会
• 页数：2
• 文件大小：1337k
• 原文格式：D
• 会议级别：全国

摘要

Objects: Conlon cancer is the third common human cancer, which is cured mainly through surgical excision and chemotherapy. Molecular target therapeutic method features in changing cancer cell properties to have more powerful antitumor function and fewer side effects toward normal cells. As a result, small molecular target medicine becomes more and more popular. Heat shock protein family, especially heat shock protein 90, is related to the stability of a number of key oncogenic client proteins such as receptor and non-receptor tyrosine kinases, and becomes very promising molecular target.17-AAG is one of the most popular HSP90 inhibitor.Our study aims to investigate the effects of 17-AAG on invasion and magiration of HCT-116 and HCT-15 cells and to clarify the related mechanisms. Methods: Scratch assay was taken to test effects of 17-AAG on migration of colon cancer cells. Transwell assay was employed to evaluate the effects of 17-AAG with different doses on invasion of HCT-116 and HCT-15 cells. The expression of E-cadherin at mRNA and protein levels was determined by RT-PCR, Western blot and immunofluorescence. Results: Treatment with 17-AAG at concentrations of 1.25, 2.5 and 5 mg/L for 48 h, significantly presented prohibition of invasion and migration in HCT-116 cells. The exposure of 17-AAG at concentrations of 1.25, 2.5, and 5 mg/L for 48 h to the HCT-116 cells significantly down-regulated the mRNA and protein expression of E-cadherin in a concentrationdependent manner. Treatment with 17-AAG at concentrations of 0.425, 0.85 and 1.7 mg/L for 48 h, significantly presented prohibition of invasion and migration in HCT-15 cells.The exposure of 17-AAG at concentrations of 0.425, 0.85, and 1.7 mg/L for 48 h to the HCT-15 cells significantly down-regulated the mRNA and protein expression of E-cadherin in a concentration-dependent manner. Conclusion: From the results, 17-AAG can prohibit invasion and migration of the two colon cancer cells, which is maybe achieved by modulating expression of E-cadherin.
Objects: Conlon cancer is the third common human cancer, which is cured mainly through surgical excision and chemotherapy. Molecular target therapeutic method features in changing cancer cell properties to have more powerful antitumor function and fewer side effects toward normal cells. As a result, small molecular target medicine becomes more and more popular. Heat shock protein family, especially heat shock protein 90, is related to the stability of a number of key oncogenic client proteins such as receptor and non-receptor tyrosine kinases, and becomes very promising molecular target.17-AAG is one of the most popular HSP90 inhibitor.Our study aims to investigate the effects of 17-AAG on invasion and magiration of HCT-116 and HCT-15 cells and to clarify the related mechanisms. Methods: Scratch assay was taken to test effects of 17-AAG on migration of colon cancer cells. Transwell assay was employed to evaluate the effects of 17-AAG with different doses on invasion of HCT-116 and HCT-15 cells. The expression of E-cadherin at mRNA and protein levels was determined by RT-PCR, Western blot and immunofluorescence. Results: Treatment with 17-AAG at concentrations of 1.25, 2.5 and 5 mg/L for 48 h, significantly presented prohibition of invasion and migration in HCT-116 cells. The exposure of 17-AAG at concentrations of 1.25, 2.5, and 5 mg/L for 48 h to the HCT-116 cells significantly down-regulated the mRNA and protein expression of E-cadherin in a concentrationdependent manner. Treatment with 17-AAG at concentrations of 0.425, 0.85 and 1.7 mg/L for 48 h, significantly presented prohibition of invasion and migration in HCT-15 cells.The exposure of 17-AAG at concentrations of 0.425, 0.85, and 1.7 mg/L for 48 h to the HCT-15 cells significantly down-regulated the mRNA and protein expression of E-cadherin in a concentration-dependent manner. Conclusion: From the results, 17-AAG can prohibit invasion and migration of the two colon cancer cells, which is maybe achieved by modulating expression of E-cadherin.

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