细胞周期蛋白E和p27在外生殖器表皮肿瘤发病中的作用

Cyclin E, p27 in the Pathogenesis of External Genital Epidermal Tumors

目的探讨细胞周期蛋白E和p27在外生殖器表皮良、恶性增殖病变中的意义。方法采用聚合酶链反应-限制性片段长度多态性分析方法,对99例外生殖器尖锐湿疣、原位鳞状细胞癌和浸润性鳞癌进行HPVDNA检测和分型,应用免疫组化方法检测上述病变中细胞周期蛋白E和p27表达。结果①上述病变中细胞周期蛋白E的表达较正常表皮显著升高,且HPV阳性组高于阴性组;比较HPV阳性的3种病变中细胞周期蛋白E表达,尖锐湿疣<原位鳞癌<浸润性鳞癌。②尖锐湿疣中p27表达较正常表皮略升高,而原位鳞癌和浸润性鳞癌中则显著下降,HPV阳性组低于阴性组,比较HPV阳性的3种病变中p27的表达,尖锐湿疣>原位鳞癌>浸润性鳞癌。③上述病变中细胞周期蛋白E与p27的表达有相关性。结论上述病变中HPV感染与细胞周期蛋白E和p27的表达有相关性,HPV可能通过影响细胞周期蛋白E和p27的表达及二者的相互作用引起感染表皮的增殖及恶变。

Objective To investigate the significance of cyclin E and p27 in genital epidermal benign and malignant tumors. Methods HPV DNA was examined and typed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) in 99 biopsy specimens taken from skin lesions of condyloma acuminatum, external genital carcinoma in situ and invasive squamous cell carcinoma. The expression of cyclin E and p27 in the lesions was examined by immunohistochemistry technique. Results (1) The cyclin E expression in epidermis was notably higher in the lesions than that in normal skin. In HPV-positive samples, the cyclin E expression was higher than that in HPV-negative ones. The cyclin E expression was strongest in invasive squamous cell carcinoma lesions and lowest in condyloma acuminatum lesions. (2) The p27 expression in condyloma acuminatum was slightly higher than that in normal epidermis. But it was notably lower in the lesions of carcinoma in situ and invasive squamous cell carcinoma than that in the normal skin. The expression was also lower in HPV-positive lesions than that in HPV-negative ones. Comparing the three kinds of HPV positive lesions, the intensity of expression was highest in condyloma acuminatum and lowest in invasive squamous cell carcinoma. (3) The study also showed that cyclin E expression was correlated with p27 expression in the lesions. Conclusions The expression of cyclin E and p27 is associated with HPV infection in the lesions. HPV infection might induce epidermal proliferation and malignant transformation by influencing the expression and interaction of cyclin E and p27.