Foxol与Ki-67在食管鳞状细胞癌组织中的表达及其意义

  目的  探讨Foxol和Ki-67蛋白在食管鳞状细胞癌组织及食管正常鳞状上皮组织中的表达及其临床意义。  方法  采用免疫组织化学SP法, 检测食管鳞状细胞癌(36例)组织及食管正常鳞状上皮(12例)组织中Foxo1和Ki-67蛋白的表达情况。  结果  Foxol蛋白在食管鳞状细胞癌及食管正常鳞状上皮组织中的阳性表达率分别为75.00%、16.67%, 而Ki-67的阳性表达率分别为83.33%、0。Foxol和Ki-67在食管鳞状细胞癌中的阳性表达率均明显高于食管正常鳞状上皮(P < 0.01)。Foxol蛋白的表达随肿瘤分化程度增高而显著增高(P < O.01), 而Ki-67的表达随肿瘤分化程度增高而降低(P=0.107)。Foxol和Ki-67蛋白的表达与其他临床病理特征无明显相关性(P > 0.05)。  结论  在食管鳞状细胞癌中, Foxol及Ki-67蛋白表达明显高于食管正常鳞状上皮组织, 且随肿瘤分化程度的增高Foxol的表达显著升高, 而Ki-67的表达则显著降低。提示Foxol和Ki-67在食管鳞状细胞癌肿瘤细胞分化过程中发挥着不同作用, 其作用机制不同。 

Expression and Significance of FoxOl and Ki-67 in Esophageal Squamous Cell Carcinoma

  Objective  To determine the expression and clinical significance of the FoxO1 and Ki-67 proteins in esophageal squamous cell carcinoma(ESCC) and normal esophageal epithelial tissue.  Methods  Streptavidin-peroxidase(SP) staining was used to detect the expression of FoxO1 and Ki-67 in 36 ESCC samples and 12 samples of normal esophageal epithelium.  Results  The positive expression rate of FoxOl was 75.00%in ESCC and 16.67%in the normal esophageal epithelium tissue.The positive expression rate of Ki-67 was 83.33%in ESCC and 0%in the normal esophageal epithelium tissue.The positive expression rates of FoxO1 and Ki-67 were significantly higher in ESCC than in normal esophageal tissue(P < 0.01).Among the ESCC cases, the rates of positive FoxO1 and Ki-67 expression were related to the degree of ESCC differentiation.The rate of positive FoxO1 expression increased as the degree of pathological differentiation increased(P < 0.01);however, the rate of positive Ki-67 expression decreased as the degree of pathologic ESCC differentiation increased(P < 0.01).No significant correlation was observed among other clinicopathologic features.  Conclusion  The positive expression rates of FoxOl and Ki-67 are significantly higher in ESCC than in normal esophageal epithelial tissue.As the degree of pathologic ESCC differentiation increases, the rate of positive FoxOl expression increases, whereas that of Ki-67 decreases. FoxO1 and Ki-67 play different roles in ESCC differentiation, and the mechanism of action is different.