Upregulation of CDK7 in gastric cancer cell promotes tumor cell proliferation and predicts poor prognosis

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• 作者：Qiuhong Wang^a ; ¹ ; Manhua Li^b ; ^f ; ¹ ; Xunlei Zhang^c ; Hua Huang^d ; Jianfei Huang^d ; Jing Ke^e ; Haifang Ding^b ; Jinzhang Xiao^c ; Xiaohang Shan^b ; Qingqing Liu^b ; Bojun Bao^b ; ^{baobojun6@163.com" class="auth_mail" title="E-mail the corresponding author} ; Lei Yang^c ; ^{leiyang.53@163.com" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Gastric cancer ; CDK7 ; Proliferation
• 刊名：Experimental and Molecular Pathology
• 出版年：2016
• 出版时间：June 2016
• 年：2016
• 卷：100
• 期：3
• 页码：514-521
• 全文大小：1485 K

文摘

CDK7 has been known as a component of CDK activating kinase (CAK) complex, the complex was composed of CDK7, Cyclin H and RING finger protein Mat1 that contribute to cell cycle progression by phosphorylating other CDKs. In addition, the complex is also an essential component of general transcription factor TFIIH which controls transcription via activating RNA polymerase II by serines 5 and 7 phosphorylation of the carboxyl-terminal domain (CTD) of its largest subunit. However, the role of CDK7 in the pathogenesis of gastric cancer has not been identified. Our study showed that CDK7 was significantly upregulated and positively correlated with tumor grade, infiltration depth, lymph node, Ki-67, and predicted poor prognosis in 173 gastric cancer specimens by immunohistochemistrical analyses. Furthermore, in vitro results indicated that CDK7 promoted proliferation of gastric cancer cells by CCK8, clone formation analyses and flow cytometric analyses, while CDK7 knockdown led to decreased cell proliferation. Our study will provide a theoretical basis for the study of CDK7 in gastric cancer.