摘要
目的:探讨雌二醇(E2)和孕酮(P)对人宫颈癌细胞(Hela细胞及Siha细胞)体外增殖及凋亡的影响。方法:体外培养人宫颈癌Hela细胞及Siha细胞,采用四甲基偶氮唑蓝(MTT)比色法检测两种激素对Hela细胞及Siha细胞增殖的影响;流式细胞仪(FCM)检测细胞生长周期和凋亡率的影响;免疫组化方法测定其雌激素受体(ER)和孕激素受体(PR)的表达。结果:E2对Hela细胞有明显促生长作用,P<0.05。P和E2+P对Hela细胞生长有抑制作用,P<0.05;对Siha细胞无明显作用,P>0.05。FCM显示,E2组He-la细胞S期细胞比例上升,凋亡率下降,P和E2+P组Hela细胞S期细胞比例下降,凋亡率上升,E2、P和E2+P组对Siha细胞的生长周期及凋亡率并无显著影响,P>0.05。E2和P对人宫颈癌细胞ER和PR的表达无显著影响。结论:E2对宫颈癌Hela细胞具有促进生长抗凋亡作用,而P抑制其生长诱导凋亡,P能有效抵消E2对Hela细胞生长的刺激作用。E2和P对Siha细胞生长无明显影响。
OBJECTIVE:To study the effects of estradiol and progesterone on the proliferation and apoptosis of Hela and Siha cervical cancer cell lines in vitro. METHODS: The proliferation of Hela and Siha cells was determined by the methyl thiazolyl tetrazolium (MTT) method. The cell apoptosis was detected by flow cytometry. The expressions of estrogen receptor(ER) and progesterone receptor (PR) were detected by immunohistochemistry. RESULTS: The growth of Hela cells was stimulated by estradiol in a dose-depended manner(P〈0.05). Progesterone or it combined with estradiol inhibited the growth of Hela cells, while no effects on Siha cells. FCM showed that estradiol increased the proportion of S phase, and reduced the apoptosis. In the progesterone group or the progesterone combined with estradiol group, the proportion of S phase was reduced and the apoptotic rate was increased, but there were no effects the cell cycle and the apoptosis on of Siha cells (P〉0.05). Estradiol and progesterone had no effect on the expressions of ER and PR of Hela and Siha cells. CONCLUSIONS: Estradiol could enhance the proliferation and inhibit the apoptosis of Hela cervical cancer cell line in vitro. Progesterone could inhibit the proliferation and induce the apoptosis. The role of estradiol combined with progesterone is remarkable than that of estradiol. Estradiol and progesterone have no effects on Siha cells.
出处
《中华肿瘤防治杂志》
CAS
2009年第6期431-433,442,共4页
Chinese Journal of Cancer Prevention and Treatment
基金
南通市社会发展科技项目(S5817)
关键词
宫颈肿瘤
雌二醇
孕酮
细胞增殖
细胞凋亡
cervix neoplasms
estradiol
progesterone
cell proliferation
apoptosis