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  • Title: [Effect of gonadotropin-releasing hormone-I agonist and gonadotropin-releasing hormone-II on endometrial carcinoma cell lines with different states of PTEN].
    Author: Zhao LJ, Wei LH, Li XP, Wang JL.
    Journal: Zhonghua Fu Chan Ke Za Zhi; 2009 Jan; 44(1):45-9. PubMed ID: 19563062.
    Abstract:
    OBJECTIVE: To study the effect of gonadotropin-releasing hormone-I (GnRH-I) agonist triptorelin and gonadotropin-releasing hormone-II (GnRH-II) on human endometrial carcinoma with different states of PTEN. METHODS: The endometrial carcinoma cells (Ishikawa, Ishikawa-PTEN, and Ishikawa-neo) were treated with different concentrations of triptorelin (10(-11) to 10(-5) mol/L) or GnRH-II (10(-11) to 10(-5) mol/L). Thirty min later, serine/threonine protein kinase (Akt) and extracellular signal-regulated kinase (ERK) 1/2 activation were detected using western blot method. 48 h later, the cell proliferation, cell cycle and apoptosis were detected using methyl thiazolyl tetrazolium (MTT) and flow cytometry. 17beta-estradiol(17beta-E2, 10(-8) mol/L) or the specific estrogen receptor (ER) antagonist, ICI182780I (10(-6) mol/L) was added. After using the two drugs: triptorelin or GnRH-II, the above parameters were detected again. RESULTS: After treated with different concentrations (10(-11), 10(-9), 10(-7), 10(-5) mol/L) of triptorelin and GnRH-II, the cell growth was slowed, the percentage of G0/G1 phase cells increased, the percentage of G2/M and S phase cells decreased and the apoptosis rate increased in a dose-dependent manner (P < 0.01, P < 0.05). These changes were more obvious in Ishikawa. The apoptosis rate induced by GnRH-II was higher than that by the same concentration of triptorelin in the three cell lines. Triptorelin and GnRH-II inhibited the Akt and ERK1/2 activity in the endometrial carcinoma cells. 17beta-E2 counteracted the effect of triptorelin and GnRH-II on the endometrial carcinoma cells (P < 0.01, P < 0.05). CONCLUSION: Triptorelin and GnRH-II can promote apoptosis rate of endometrial carcinoma cells and inhibit cell proliferation in a dose-dependent manner which may be caused by ERK1/2 and Akt activity inhibition, and is related to the status of PTEN and could be offset by 17beta-E2.
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