摘要
目的 分析Ki-67、Survivin和Livin蛋白在结肠腺上皮中的表达,探讨其在结肠腺癌发生、发展过程中增殖能力的变化和抗凋亡因素的影响.方法 取结肠腺上皮轻度非典型增生36例,中度非典型增生34例,重度非典型增生18例,高分化腺癌35例,中分化腺癌27例,低分化腺癌35例,癌旁组织34例.采用免疫组织化学方法结合组织芯片技术分别检测Ki-67、Survivin和Livin蛋白在不同组间的表达.结果 结肠上皮轻度非典型增生、中度非典型增生、重度非典型增生、高分化腺癌、中分化腺癌、低分化腺癌和癌旁组织Ki-67的阳性表达率为（21.56±19.20）％、（37.44±17.41）％、（36.17±17.41）％、（55.29±16.13）％、（44.89±29.67）％、（45.11 ±29.24）％及（43.94±28.84）％,Ki-67在各组间表达差异有统计学意义（F=6.796,P＜0.05）.Survivin和Livin阳性表达率分别为：13.8％、44.1％、77.8％、85.7％、85.1 ％、91.4 ％、91.1％和2.7％、38.2％、55.6％、100.0％、77.8％、80.0％、79.4％.Survivin和Livin在各组间表达差异有统计学意义（X2值分别为84.754、95.200,P＜0.05）.Livin与Ki-67表达有相关性（r=0.360,P＜0.05）,而Survivin与Ki-67表达无相关性（r=0.044,P＞0.05）.结论 结肠腺上皮从轻度非典型增生到高分化腺癌细胞增殖形成一个高峰,又逐渐下降到低分化腺癌形成一个平台.结肠上皮发生癌变时,细胞的增殖能力显著增强,凋亡抑制也达高峰,肿瘤细胞发生了恶性生物学行为的转变；结肠癌周微环境使得癌旁组织增殖能力增强,进一步促进肿瘤的发生、发展；Livin能够抑制凋亡,而且与Survivin协同作用,在结肠腺癌发生、发展中发挥一定的作用.
Objective To investigate the expression of Ki-67,Survivin,Livin in dysplasia,colon carcinogenesis and para-carcinoma tissues,and to discuss the variation of cell proliferous capability in colon carcinogenesis and antiapoptosis factors.Methods 219 specimens were composed of mild,moderate and severe atypical hyperplasia,well,moderately,poorly differentiated adenocarcinoma,para-carcinoma tissues of 36,34,18,35,27,35 and 34 cases.Detected the expression of Ki-67,Survivin and Livin with tissue microarray and immunohistochemical methods.All data were statistically analyzed by SPSS 17.0.Results In mild,moderate and severe atypical hyperplasia,well,moderately,poorly differentiated adenocarcinoma and para-carcinoma tissues the expression of Ki-67 were （21.56 ± 19.20）%,（37.44 ± 17.41）%,（36.17 ± 17.41）%,（55.29 ± 16.13）%,（44.89 ± 29.67）%,（45.11 ± 29.24）%,（43.94 ± 28.84）%,Survivin were 13.8 %,44.1%,77.8 %,85.7 %,85.1%,91.4 %,91.1%,and Livin were 2.7 %,38.2 %,55.6 %,100.0 %,77.8 %,80.8 %,79.4 %.The differences of Ki-67,Survivin and Livin expression in each group were statistically significant （F =6.796,X2 =81.754,X2 =95.200,all P 〈 0.05）.Ki-67 was significantly correlated with expression of Livin （r =0.360,P 〈 0.05） and no correlated with expression of Survivin （r =0.044,P 〉 0.05）.Conclusion Colonic epithelium from mild atypical hyperplasia to proliferation of well-differentiated adenocarcinoma cells formed a peak,and gradually down to poorly differentiated adenocarcinoma formed a platform.When the colon epithelial cells to become cancerous,the capability of cell proliferation will significantly enhance,apoptosis inhibition will reach the peak and the tumor cell will happen the changes of malignant biological behavior.Tumor microenvironment may promote the cell proliferation in para-carcinoma tissues and the development of colon cancer.Livin may inhibit apoptosis and promot the progression in synergistic mechanism importing with Survivin,which play a role in the development
出处
《肿瘤研究与临床》
CAS
2013年第5期316-319,共4页
Cancer Research and Clinic
基金
基金项目：云南省科技厅-昆明医科大学应用基础研究联合基金（2008CD004R）
