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Inhibition of Pim-1 attenuates the proliferation and migration in nasopharyngeal carcinoma cells

Inhibition of Pim-1 attenuates the proliferation and migration in nasopharyngeal carcinoma cells

作     者:Wei Jie Qi-Yi He Bo-Tao Luo Shao-Jiang Zheng Yue-Qiong Kong Han-Guo Jiang Ru-Jia Li Jun-Li Guo Zhi-Hua Shen 

作者机构:Department of Pathology & PathophysiologySchool of Basic Medicine ScienceGuangdong Medical College Hainan Provincial Key Laboratory of Tropical MedicineHainan Medical College 

出 版 物:《Asian Pacific Journal of Tropical Medicine》 (亚太热带医药杂志(英文版))

年 卷 期:2012年第5卷第8期

页      面:645-650页

核心收录:

学科分类:1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基  金:supported by grants from the Doctoral Program of Guangdong Medical College(B2010013) National Natural Science Foundation of China(81000073) Natural Foundation of Hainan Province of China 1811197, 310043,and 811201) 

主  题:Nasopharyngeal carcinoma Pim-1 Quercetagetin Cell proliferation Cell migration 

摘      要:Objective:To explore the role of proto-oncogene Pim-1 in the proliferation and migration of nasopharyngeal carcinoma(NPC) ***:Pim-1 expressions in NPC cell lines CNE1,CNE1-GL,CNE-2Z and C666-1 were examined by KT-PCR,western blotting and immunoflucesence,*** CNE1,CNE1-GL and C666-1 cells were treated with different concentrations of Pim-1 special inhibitor,quercelagetin,the cell viability,colony formation rate and migration ability were ***:Pim-1 expression was negative in well-differentiated CNE1 cells,whereas expressed weakly positive in poor-differentiated CNE-2Z cells and strongly positive in undifferentiated C666-1 ***,CNE1-GL cells that derived from CNE1 transfected with an Epstein Barr virus latent membrane protein-1 over-expression plasmid displayed stronger expression of *** of CNE1-GL and C666-1 cells with quercelagetin significantly decreased the cell viability,colony formation rate and migration ability but not the CNE1 ***:These findings suggest that Pim-1 overexpression contributes to NPC proliferation and migration,and targeting Pim-1 may be a potential treatment for anti-Pim-1-expressed NPCs.

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