Id2 regulates the proliferation of squamous cell carcinoma in vitro via the NF-κB/Cyclin D1 pathway  

作　　者：Chuan Wang Qiang Chen Yuki Hamajima Wei Sun Yi-Qing Zheng Xiao-Hua Hu Frank G. Ondrey Ji-Zhen Lin 

机构地区：[1]The Cancer Center and Fujian Key Laboratory of Translational Cancer Medicine, Union Hospital, Fujian Medical University, Fuzhou, Fujian 350001, P. R. China [2]Department of Otolaryngology Head and Neck Surgery, University of Nagoya City, Nagoya 460-0002, Japan [3]Department of Otolaryngology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, Guangdong 510120, P. R. China [4]Department of Otolaryngology and Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA

出　　处：《Chinese Journal of Cancer》2012年第9期430-439,共10页

摘　　要：Squamous cell carcinoma (SCC) is a significant cause of cancer morbidity and mortality worldwide, with an incidence of up to 166 cases per 100 000 population. It arises in the skin, upper aerodigestive tract, lung, and cervix and affects more than 200 000 Americans each year. We report here that a microarray experiment comparing 41 SCC and 13 normal tissue specimens showed that Id2, a gene that controls the cell cycle, was significantly up-regulated in SCC. Enforced expression of Id2 in vitro stimulated the proliferation of SCC cells and up-regulated the transcription of nuclear factor kappa B (NF-κB) and cyclin D1. Enhancement of the NF-κB activity with p65 significantly increased the cell proliferation and the transcription of cyclin D1, whereas inhibition of the NF-κB activity with I kappa B alpha mutant (IκBα M) and pyrroline dithiocarbamate (PDTC) abrogated cell proliferation and transcription of cyclin D1. Furthermore, a mutated NF-κB binding site in the cyclin D1 promoter fully abrogated the Id2-induced transcription of cyclin D1. Taken together, these data indicate that Id2 induces SCC tumor growth and proliferation through the NF-κB/cyclin D1 pathway.Squamous cell carcinoma （S CC） is a significant cause of cancer morbidity and mortality worldwide, with an incidence of up to 166 cases per 100 000 population. It arises in the skin, upper aerodigestive tract, lung, and cervix and affects more than 200 000 Americans each year. We report here that a microarray experiment comparing 41 SCC and 13 normal tissue specimens showed that Id2, a gene that controls the cell cycle, was significantly up-regulated in SCC. Enforced expression of Id2 in vitro stimulated the proliferation of SCC cells and up-regulated the transcription of nuclear factor kappa B （NF-kB） and cyclin DI. Enhancement of the NF-KB activity with p65 significantly increased the cell proliferation and the transcription of cyclin D1, whereas inhibition of the NF-kB activity with I kappa B alpha mutant （IkBα M） and pyrroline dithiocarbamate （PDTC） abrogated cell proliferation and transcription of cyclin D1. Furthermore, a mutated NF-KB binding site in the cyclin D1 promoter fully abrogated the Id2- induced transcription of cyclin DI. Taken together, these data indicate that Id2 induces SCC tumor growth and proliferation through the NF-kB/cyclin D1 pathway.

关 键 词：鳞状细胞癌 体外增殖 细胞周期蛋白D1 核因子KAPPA 二硫代氨基甲酸盐 cyclin NF-KB NF-KB 

分 类 号：Q253[生物学—细胞生物学] S858[农业科学—临床兽医学]