Abstract

Objective To investigate the expression of PLAGL2 in colon cancer tissues and adjacent normal tissues and its relationship with the clinicopathological factors of colon cancer, to study the function of PLAGL2 on invasive process of colon cancer cells and its mechanism. Methods The expressions of PLAGL2 were detected in 40 fresh colon cancer tissues and control normal tissues by immunohistochemistry. According to the results of preoperative imaging examinations and postoperative pathological staging of patients, the relationship between the expression of PLAGL2 and the clinicopathological factors was analyzed. After construction of the recombinant plasmid pcDNA3.1-PLAGL2, SW480 cells were transfected with the plasmid pcDNA3.1- PLAGL2 and empty vector using Lipofectamine™ 2000. Three groups of cell line including SW480, Vector and PLAGL2 were cultured and compared the difference of invasive ability by Transwell assay. Finally, Western-blot detected the expression of E-cadherin, vimentin and MMP-7 among cell line of the three groups. Results The immunoreactivity scores of PLAGL2 in stage Ⅲ-Ⅳ, stage Ⅰ-Ⅱ and adjacent normal tissues were 8.12±2.997、5.71±2.494、2.17±0.984 respectively, indicating a statistically significant difference (F=64.225, P<0.01). Chi square test showed that the patients with PLAGL2-over expression had more advanced stages (χ2=5.700, P=0.017)、bigger sizes (χ2=8.174, P=0.008) and easier to happen metastasis (χ2=13.610, P<0.001). The invasion of the cells were significantly promoted in PLAGL2 group than other two groups by Transwell assay (F=27.997, P<0.01). Western-blot method for detection of PLAGL2 cells significantly decreased expression of E-cadherin (F=38.461, P<0.01) and increased the expression of vimentin (F=28.741, P<0.01) and MMP-7 (F=24.520, P<0.01), with statistically significant difference compared other two groups. Conclusions The upregulation of PLAGL2, which is closely correlated to the occurrence and development of colon cancer and can promote the invasive ability of colon cancer cells, may be related to the formation of EMT. Key words: Colonic neoplasms; Pleomorphic adenoma gene like-2; Epithelial mesenchymal transition; Invasion

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