Polo样激酶1在结肠直肠癌组织中的表达及其在结肠直肠癌细胞增殖中的作用

目的：探讨Polo样激酶1（PLK1）在结肠直肠癌组织中的表达及体外RNA干扰抑制plk1对结肠直肠癌细胞增殖的影响。方法：应用免疫组化法测56例结肠直肠癌病人的癌组织和癌旁正常组织中PLK1及PCNA的表达;用Western印迹法测肠癌主要细胞株中PLK1的表达;针对plk1基因设计3条小干扰RNA片段,瞬时转染高表达结肠直肠癌细胞株,采用实时定量PCR及Western印迹法测转染后PLK1的基因及蛋白的表达水平;CCK-8法测细胞增殖能力。结果：结肠直肠癌组织中PLK1、PCNA的表达明显高于癌旁正常组织（P〈0.05）,两者的表达与肿瘤大小、TNM分期、淋巴结转移和浸润深度均有相关性（P〈0.05）,且两者间的表达呈正相关（P〈0.05）。Western印迹法筛选出SW1116细胞株PLK1表达最高,下调PLK1表达后,其增殖能力较对照组都有所下降（P〈0.05）。结论：PLK1在结肠直肠癌组织中呈过表达,可能在结肠直肠癌细胞增殖调节失衡中起重要作用,并进一步促进其迁移和浸润,其有望成为评估结肠直肠癌进展及预后的一个重要指标。

Expression of PLK1 in colorectal carcinoma and influence of PLK1 expression on proliferation of colorectal carcinoma cells

Objective To investigate PLK1 expression in colorectal carcinoma and influence of PLK1 expression on proliferation of colorectal carcinoma cells.Methods The expression of PLK1 in colorectal carcinoma was detected by S-P immunohistochemistry in 56 cases of colorectal carcinoma tissue and adjacent normal tissue.The expression of PLK1 in main colorectal carcinoma cell lines was detected by Western-blot assay.3 small interfering RNA targeting plk1 were designed and transfected into colorectal carcinoma celllines.Expression of PLK1 mRNA and protein after transfection were detected by real time PCR and Western-blot assay.The proliferation was assayed by CCK-8 assay.Results The expression of PLK1 with PCNA between colorectal carcinoma and adjacent normal tissue was significantly different（P 0.05）.PLK1 and PCNA expression level had correlation with tumor size,lymph node metastasis,invasion depth and TNM stage（P0.05）.The expression of PLK1 in colorectal cancer tissue was positively correlated with that of PCNA（P0.05）.Our Western-blot assay result shows that carcinoma cell line SW1116 expresses the highest quantity of PLK1 of all the cell lines we choosed,and when PLK1 is down-regulated after transfection in cell line SW1116,its proliferation was obviously suppressed compared with control groups（P0.05）.Conclusions PLK1 may play a key role in the hyperplasia of colorectal carcinoma,which may further lead to motivation and invasion of CRC cell.