摘要
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 expression of CKIP - 1 and p - Akt protein in colorectal carcinoma and the correlation be- tween their expression and clinical pathological characteristics and prognosis, as well as the possible role of CKIP - 1 in PI3 K/Akt path- way. Methods CKIP - 1 and p - Akt protein expression was determined in 50 colorectal cancerous tissues and it＇s corresponding normal paracancerous tissues, as well as 31 colorectal adenoma tissues by immunohistoehemistry （IHC） research. Results CKIP - 1 protein was localized mainly in plasma and cell membrane, although faint staining was also observed in nuclear. The positive rate was 73% in cancer- ous tissues, which was significantly lower than paracancerous tissues（ 1100% , P 〈 0.01 ）. The positive rate of CKIP - 1 was 87. 1% in adenoma tissues（P 〈 0.05） ,which was significantly lower than paracancerous tissues, p -Akt protein immunoreaetivity was found mainly in the nuclear, and faint staining was also found in the plasma. The positvely rate was 80% in cancerous tissues, 58.1% in adenoma tis- sues, and 16% in paraeancerous tissues. Clinicopathological analysis revealed that CKIP -1 expression was significantly correlated with the degree of differentiation of colorectal cancer, and p- Akt expression was significantly correlated with the degree of differentiation and the TNM classification. The expression of CKIP - 1 was negatively correlated with the expression of p - Akt. Conclusion CKIP - 1 was involved in the development of colorectal cancer and may inhibit colorectal development throuth the inhibition of PI3 K/Akt pathway.
出处
《医学研究杂志》
2013年第2期63-67,共5页
Journal of Medical Research
