p57 kip2和细胞周期蛋白E在体外培养人子宫内膜癌JEC细胞中的表达

Expressions of p57 kip2 and cyclin E in human endometrial carcinoma cell line JEC cultured in vitro

目的探讨p57 kip2和细胞周期蛋白E在体外培养人子宫内膜癌JEC细胞中的表达,并分析雌二醇(E_2)对其的影响。方法分别采用低浓度(10^(-6)mol/L)、中浓度(10^(-8)mol/L)、高浓度(10^(-10)mol/L)的E_2对在体外培养的人子宫内膜癌JEC细胞进行处理,处理时间为1 d、2 d、3 d,处理完毕后采用Western Blot技术观察p57 kip2和细胞周期蛋白E的表达情况。结果Western Blot技术结果显示,JEC细胞经E_2处理1 d后,p57 kip2在高浓度组的表达水平最好,在中浓度组的表达水平最差,差异有统计学意义(P<0.01);细胞周期蛋白E在高浓度组的表达水平最差,在中浓度组的表达水平最好,差异有统计学意义(P<0.01)。JEC细胞经E_2处理2 d、3 d后,p57 kip2和细胞周期蛋白E的表达量随E_2处理浓度的升高而加大,差异均有统计学意义(均P<0.05)。p57 kip2和细胞周期蛋白E的表达互不影响(r=-0.01,P=1.02)。结论 p57 kip2和细胞周期蛋白E在EC发生、发展中的作用均受到E_2的影响。JEC细胞经E_2处理浓度越高及时间越长,其将由正常生长繁殖状态转变成生长繁殖抑制状态。

Objective To explore the expressions of p57 kip2 and cyclin E in human endometrial carcinoma cell line JEC cultured in vitro,analyze the effect of estradiol（ E2）. Methods Human endometrial carcinoma cell line JEC cultured in vitro was treated by different doses of E2（ 10^-6mol/L,10^-8mol/L,10^-10mol/L） for 1,2,and 3 days,respectively. After treatment,Western Blot was used to observe the expressions of p57 kip2 and cyclin E. Results Western Blot results showed that after treated by E2 for one day,the expression level of p57 kip2 in high dose group was the best,while the expression level of p57 kip2 in moderate dose group was the worst,there was statistically significant difference（ P〈0. 01）; the expression level of cyclin E in high dose group was the worst,while the expression level of cyclin E in moderate dose group was the best,there was statistically significant difference（ P〈0. 01）; after treated by E2 for 2 and 3 days,the expression levels of p57 kip2 and cyclin E increased with the increase of E2 dose,there were statistically significant differences（ P〈0. 05）. There was no correlation between p57 kip2 expression and cyclin E expression（ r =-0. 01,P = 1. 02）. Conclusion p57 kip2 and cyclin E are affected by E2 in oncogenesis and development of endometrial carcinoma,with the increase of E2 dose and time extension of treatment,JEC cells transform from normal growth and reproduction state to growth and reproduction inhibition state.