He et al. Journal of Experimental & Clinical Cancer Research 2011, 30:109 http://www.jeccr.com/content/30/1/109 R E S E A R C H Open Access Effects of cyclin-dependent kinase 8 specific siRNA on the proliferation and apoptosis of colon cancer cells Song-Bing He1, Yin Yuan1, Lei Wang1, Min-Jing Yu1, Yi-Bei Zhu2 and Xing-Guo Zhu1* Abstract Background: To investigate the expression of cyclin-dependent kinase 8 (CDK8) and b-catenin in colon cancer and evaluate the role of CDK8 in the proliferation, apoptosis and cell cycle progression of colon cancer cells, especially in HCT116 cell line. Methods: Colon cancer cell line HCT116 was transfected with small interfering RNA (siRNA) targeting on CDK8. After CDK8-siRNA transfection, mRNA and protein expression levels of CDK8 and b-catenin were determined by reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot assay in HCT116 cells. Cell proliferation was measured by 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide Methylthiazolyl tetrazolium (MTT) assay, and cell cycle distribution and apoptosis were analyzed by flow cytometry analysis (FACS). CDK8 and b- catenin protein levels were also examined by real-time PCR and immunohistochemistry (IHC) in colon cancer tissues and adjacent normal tissues. Results: After CDK8 specific siRNA transfection, mRNA and protein expression levels of CDK8 and b-catenin in HCT116 cells were noticeably decreased (P < 0.05). CDK8 specific siRNA transfection inhibited HCT116 cells’ proliferation and facilitated their apoptosis significantly (P < 0.05). In addition, the proportion of HCT116 cells in the G0/G1 phase was remarkably increased after CDK8-siRNA transfection (P < 0.05). The expression levels of CDK8 and b-catenin in adjacent normal tissues were lower than in tumor tissues (P < 0.05). Moreover, the expression of CDK8 was correlated with the expression of b-catenin in both tumor and adjacent normal tissues (P < 0.05). Conclusions: CDK8 and b-catenin were expressed in colon cancer at a high frequency. CDK8 specific siRNA transfection down-regulated the expression of CDK8 in colon cancer cells, which was also associated with a decrease in the expression of b-catenin Moreover, CDK8 specific siRNA inhibited the proliferation of colon cancer cells, promoted their apoptosis and arrested these cells in the G0/G1 phase. Interference of CDK8 might be an effective strategy through b-catenin regulation of colon cancer. Background Colon cancer is a result of an evolving process charac- terized by alterations of multiple genes and dysregulated cell signal transduction pathways. It has been well known that mutations of key genes in the Wnt/b-cate- nin signaling pathway play an important role in the occurrence and development of colon cancer [1,2]. Under physiological conditions, Wnt contributes to the stabilization of b-catenin. Once stabilized, b-catenin * Correspondence: zxg45@hotmail.com 1Department of General Surgery, the First Affiliated Hospital of Soochow University, 215006 Suzhou, Jiangsu Province, China Full list of author information is available at the end of the article accumulates and migrates to the nucleus. On the other hand, when the level of b-catenin within the cytoplasm surpasses the threshold, the molecule migrates to the nucleus, binds to the transcription factor, and exposes the promoters of downstream genes, such as c-myc, cyclinD1, survivin, gastrin, vascular endothelial growth factor (VEGF), and associated exchange factors (Asef). Finally, these activated genes contribute to abnormal cellular proliferation [3,4]. Cyclin-dependent kinase (CDK) 8 is located in chro- mosome 13q12.13 and is a member of the CDK family [5,6]. CDK is classified as a serine-threonine protein kinase, and ten of its members have been identified in © 2011 He et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.