Tuyển tập các báo cáo nghiên cứu về hóa học được đăng trên tạp chí sinh học đề tài : Protein kinase CK2a is overexpressed in colorectal cancer and modulates cell proliferation and invasion via regulating EMT-related genes | Zou et al. Journal of Translational Medicine 2011 9 97 http content 9 1 97 JOURNAL OF TRANSLATIONAL MEDICINE RESEARCH Open Access Protein kinase CK2a is overexpressed in colorectal cancer and modulates cell proliferation and invasion via regulating EMT-related genes Jinjin Zou1 Hesan Luo1 Qin Zeng1 Zhongyi Dong1 Dehua Wu1 and Li Liu2 Abstract Background Protein kinase CK2 is a highly conserved ubiquitous protein serine threonine kinase that phosphorylates many substrates and has a global role in numerous biological and pathological processes. Overexpression of the protein kinase CK2a subunit CK2a has been associated with the malignant transformation of several tissues with not nearly as much focus on the role of CK2a in colorectal cancer CRC . The aims of this study are to investigate the function and regulatory mechanism of CK2a in CRC development. Methods Expression levels ofCK2a were analyzed in 144 patients 104 with CRC and 40 with colorectal adenoma by immunohistochemistry. Proliferation senescence motility and invasion assays as well as immunofluorescence staining and western blots were performed to assess the effect of CK2a in CRC. Results The immunohistochemical expression of nuclear CK2a was stronger in tumor tissues than in adenomas and normal colorectal tissues. Suppression ofCK2a by small-interfering RNA or the CK2a activity inhibitor emodin inhibited proliferation of CRC cells caused G0 G1 phase arrest induced cell senescence elevated the expression of p53 p21 and decreased the expression of C-myc. We also found that knockdown of CK2a suppressed cell motility and invasion. Significantly CK2a inhibition resulted in p-catenin transactivation decreased the expression levels of vimentin and the transcription factors snail1 and smad2 3 and increased the expression of E-cadherin suggesting that CK2a regulates the epithelial-mesenchymal transition EMT process in cancer cells. Conclusions Our results indicate that CK2a plays an .
