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Effects Of The Selective Inhibitor Of COX-2 NS-398 In Human Ovarian Cancer Cell Lines C13K And Its Influence On The Expression Of Snail And E-cadherin.

Posted on:2011-09-01Degree:MasterType:Thesis
Country:ChinaCandidate:C X SunFull Text:PDF
GTID:2144360305465849Subject:Obstetrics and gynecology
Abstract/Summary:PDF Full Text Request
Objective:To investigate the effects of the selective inhibitor of cyclooxygenase-2 (COX-2) NS-398 on the proliferation in Cisplatin-resistant human ovarian cancer cell lines C13K in vitro, and to explore its influence on the expression of snail and E-cadherin.Methods:Cisplatin-resistant human ovarian cancer cell lines C13K were cultured in vitro respectively under the irritation of NS-398 with different concent rations (50,100,200μmol/L) for 48h and 72h. The cell growth state were observed Under the inverted microscope. The inhibition rates were detected by methyl thiazolyl tetrazolium (MTT). The expressions of Snail mRNA and E-cadherin mRNA were detected by Real-time PCR, the Snail protein and E-cadherin protein were detected by immunohistochemical method (SABC).Results:The results of MTT showed that NS-398 significantly inhibited the proliferation of ovarial cancer cell in a dose and time dependentmanner. NS-398 at 200μmol/L obviously inhibited the proliferation of C13K cell, and there was significant difference between the experimental groups and the control groups (P< 0.05). By RT-PCR and immunohistochemical method, the alteration of Snail mRNA and protein decreased after administration of NS398 for 48h and 72h,but the alteration of E-cadherin mRNA and protein increased.The difference was significant between the experimental groups and the control groups. (P<0.05).Conclusion:The selective inhibitor of COX-2 NS-398 can inhibit proliferation of Cisplatin-resistant human ovarian cancer cell lines C13K via downregulating the expression of Snail and upregulating the expression of E-cadherin.
Keywords/Search Tags:Ovarian cancer, cyclooxygenase-2, NS398, Snail, E-cadherin
PDF Full Text Request
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