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目的研究CKIP-1与大肠癌的发生发展、预后的关系及与PI3K/Akt通路的相关性,为大肠癌及分子靶向治疗提供可能的靶点。方法收集大肠癌患者手术标本,通过免疫组化方法检测CKIP-1蛋白、p-Akt蛋白在大肠癌组织中的表达;分析CKIP-1的表达与大肠癌临床病理参数、p-Akt表达的相关性。结果 CKIP-1蛋白主要位于胞质及包膜上,部分位于胞核;CKIP-1蛋白在大肠癌组织中的阳性表达率显著低于癌旁正常组织;CKIP-1在腺瘤组织中的表达率显著低于癌旁正常组织。p-Akt阳性染色大部分定位于胞核;少部分也定位于胞质;p-Akt在大肠癌组织中的表达明显高于腺瘤组织,p-Akt在腺瘤组织中的表达明显高于癌旁正常组织,3者均具有显著性差异。CKIP-1的表达与大肠癌的分化程度显著相关,p-Akt的表达与大肠癌的分化程度、临床分期显著相关。在大肠癌中,CKIP-1蛋白的表达与p-Akt蛋白的表达呈负相关。结论 CKIP-1可能参与了大肠癌的发生发展,并可能通过下调PI3K/Akt介导的细胞信号转导通路发挥作用。
Objective To investigate the relationship between the expression of CKIP-1, the prognosis and the PI3K / Akt pathway in colorectal cancer and provide a possible target for colorectal cancer and molecular targeted therapy. Methods The specimens of patients with colorectal cancer were collected. The expression of CKIP-1 protein and p-Akt protein in colorectal cancer tissues were detected by immunohistochemistry. The correlation between the expression of CKIP-1 and the clinicopathological parameters and the expression of p-Akt in colorectal cancer was analyzed Sex. Results CKIP-1 protein mainly localized in the cytoplasm and envelope, and partly located in the nucleus. The positive rate of CKIP-1 protein in colorectal carcinoma was significantly lower than that in adjacent normal tissues. The expression of CKIP-1 in adenoma tissues The rate was significantly lower than the adjacent normal tissue. Most of p-Akt positive staining located in the nucleus; some also located in the cytoplasm; p-Akt in colorectal cancer tissue was significantly higher than adenoma, p-Akt in adenoma was significantly higher than Adjacent normal tissue, 3 were significant differences. The expression of CKIP-1 was significantly correlated with the degree of differentiation of colorectal cancer. The expression of p-Akt was significantly associated with the degree of differentiation and clinical stage of colorectal cancer. In colorectal cancer, CKIP-1 protein expression and p-Akt protein expression was negatively correlated. Conclusion CKIP-1 may be involved in the development of colorectal cancer and may play a role by down-regulating PI3K / Akt-mediated cell signal transduction pathway.