Effection Of FSH On Proliferation Of The Ovarian Epithelial Cancer

Ovarian cancer causes more deaths than any other cancer of the female reproductive system in the United States. Although all cell types of the human ovary may undergo neoplastic transf- ormation, the majority of tumors (80%~90%) are derived from the ovarian surface epithelium. Epidemiological data show that the risk of epithelial ovarian cancer is decreased by pregnancy and oral contraceptive use, and increased in women over the age of 45 years. On this basis, it has been proposed that repetitive ovulatory trauma and high circulating concentrations of follicle stimulating hormone (FSH) and luteinizing hormone (LH) may contribute to cancer dedevelopment or progression. Experimental models of ovarian cancer support a role for repeated epithelial trauma-repair and gonadotropin stimulation in the development and progression of ovarian cancer. Follicle stimulating hormone (FSH) is secreted by the pituitary gonadotropin cells in the reproductive stage of the main physiological role is to promote follicle growth and development. From the menopausal transition, FSH significantly increased in the female serum,and maitain the high level more than 10 years,just in this period showed the high incidence of ovarian cancer, this phenomenon has caused widespread concern in domestic and foreign scholars. FSH receptors (FSH-R) are expressed by normal ovarian surface epithelial cells, as well as by epithelial ovarian carcinoma cells and ovarian cancer cell lines. Moreover, FSH can effect the activating pathways associated with cell proliferation and oncogenesis in normal and malignant ovarian surface epithelial cells .Objective:Early experiments have proved that FSH obviously promote the proliferation effect on cultured human ovarian serous adenocarcinoma cell line HO8910. The study was designed to prove FSH to promoting the growth of ovarian cancer cells in nude mice HO8910.Materials and Methods: Cultured human ovarian serous adenocarcinoma cell line HO8910, 20 cases of ovarian cancer in nude mice to establish subcutaneous tumor models were divided into 4 groups, n = 5; A,B grous (castrated groups) were inoculated with HO8910 cell; C,D groups( not receive castration groups) were also inoculated HO8910 cell, A,C groups as the experimental group, B,D groups as control group. The nude mouse of A,C groups was injected intraperitoneally every other day FSH 10 U. B,D group injected with 0.9% nacl every other day. The effection of FSH with FSHR on HO8910 cells were detected by fluorescence ,and the tumor morphology as well as its growth rate were observed using immunohistochemical techniques, HE staining .Results: We using HO8910 cells established the FSH with FSHR interrection model in nude mice. the growth rate of the exparimental groups A,C increased significantly (P <0.05) compared with the groups B,D; and in the first 16～36 days of nude mice in experimental groups Volume growth rate was faster than the control groups; Immunohistochemical analysis showed that the expression levels of the FSHR in the tumor tissue of A,C groups higher than that of the control groups; Growth inhibitory factor receptor TβRII was higher (P <0.05) in the experimental groups, but growth inhibitory factor TβRⅠslightly lower in the experimental groups than in the control groups, But there is no statistical significance.Conclusions:The expression of FSHR in HO8910 cells confirmed by fluorescence . The tumor mass growth rate was faster in experimental groups than that of in control groups especially in the first 16～36 days.And confirmed that first ,FSH conbing with FSHR can directly promote the proliferation of ovarian cancer cell; Second,it also can change the expression of TGF-βand diminish its inhibity effects.