结直肠癌PTEN基因表达及与p-ERK相关性研究

目的 研究结直肠癌中的PTEN、p-ERK蛋白的表达及相互关系,初步探讨它们在结直肠癌的发生发展中的生物学意义.方法 应用免疫组织化学染色快捷法,检测40例结直肠癌组织、18例结直肠腺瘤、13例结直肠正常黏膜中PTEN蛋白、和p-ERK蛋白的表达情况,比较PTEN蛋白表达与临床病理指标的关系,及其与p-ERK蛋白表达的相关性.结果 1.结直肠癌癌组织PTEN蛋白表达的阳性率(57.5％)明显弱于腺瘤(72.2％)及正常组织(100％),组间比较差异有显著性(P＜0.05),其表达水平与结直肠癌的分化程度、淋巴结转移、浸润深度、Dukes分期有关,与患者的性别、年龄,肿瘤大小及位置无关(P＞0.05)2.结直肠癌组织p-ERK蛋白表达的阳性率(72.5％)明显高于正常结直肠黏膜组(0.00％)及腺瘤组(66.6％),组间比较差异有显著性(P＜0.01),其表达随结直肠癌侵润深度增加、淋巴结转移、Duke分期的进展而增高.3.PTEN蛋白表达强度与p-ERK蛋白表达强度之间呈负相关(r=-0.452,P＜0.05).结论 提示抑癌基因PTEN的表达与结直肠癌生物学行为密切相关；在结直肠癌发生、发展过程中,可能由于PTEN蛋白的低表达或失表达不能有效抑制ERK磷酸化,使细胞发生癌变,并促进癌变细胞的浸润、转移.

Expression of PTEN and its relationship withp-ERK in colorectal cancer

Objective To study the expression of Phosphatase and tensin homology deleted on chromosome ten （PTEN） and p-ERK protein in eolorectal cancer,and their correlations with the progression of colorectal cancer. Methods PTEN and p-ERK protein expressions were detected by immunohistochemical method in 40 cases of colorectal cancer, 18 cases of colorectal adenoma, and 13 cases of normal colorectal tissues. PTEN protein expression was compared with clinico pathologic parameters as related to p ERK. Results 1. The positive rate of PTEN was significantly lower in colorectal cancer（57.5 % ） than in colorectal adenomas（72.2 %） and normal tissue（100%）（P〈0.05）. The expression of PTEN was associated with the loss of tumor differentiation, lymphnode metastasis, invasion depth and Dukes stage （P〈0.05）, but not with patients＂ sex,age,tumor location and tumor size. 2. The positive rate of p-ERK was higher in colorectal cancer （72.5%） than in colorectal adenomas （66.6%） and normal tissues （0.00%）（P〈0.01） ,and related with the development of tissue invasiveness, lymphnode metastasis and Dukes stage. 3. There was a significant negative correlation between PTEN and p-ERK （r =-0. 452, P〈 0. 05）. Conclusion The date suggest that the expression level of PTEN protein is closely related to biological behavior of colorectal cancer. Decrease or deletion of PTEN protein expression may be unable to inhibit ERK phosphorylation, which will result in carcinogenesis,invasiveness and metastasis.