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Expression And Significance Of Glucocorticoid Receptor In Endometrial Carcinom

Posted on:2022-03-17Degree:MasterType:Thesis
Country:ChinaCandidate:J C MaFull Text:PDF
GTID:2504306314462074Subject:Obstetrics and gynecology
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BackgroundEndometrial cancer is a common malignant tumor of the female.The incidence rate is increasing worldwide.Most of these cancers are directly related to the persistent estrogen stimulation without estrogen.Obesity,hypertension and diabetes are common risk factors.The occurrence of tumor is closely related to immunity.The occurrence of tumor is closely related to immunity.High dose of glucocorticoid has immunosuppressive effect.Long term application may be related to the occurrence of tumor.Endometrial cancer incidence rate is high and closely related to hormones.In recent years,glucocorticoid receptor has been reported to be related to the development of cancer.Its antagonist,mifepristone,is also used in cancer treatment and has certain curative effect.However,there are few studies on glucocorticoid receptor and its antagonist in endometrial cancer,and the mechanism is not clear.It may be helpful for the diagnosis and treatment of endometrial cancer to study glucocorticoid and endometrial cancer from the perspectives of immunity and hormone.ObjectiveTo study the expression of glucocorticoid receptor in endometrial carcinoma;Objective to study the effect of glucocorticoid and its antagonist on tumor in vivo and in vitro,and explore its possible molecular pathway.MethodsThe expression of glucocorticoid receptor in endometrial carcinoma and normal endometrium was detected by immunohistochemistry;Dexamethasone,a glucocorticoid receptor agonist,and mifepristone,an antagonist of dexamethasone,were used to treat Ishikawa cells,then the proliferation of Ishikawa cells was detected by CCK-8 method.Dexamethasone,a glucocorticoid receptor agonist,and mifepristone,an antagonist of dexamethasone,were used to treat Ishikawa cells,then the invasion and migration of Ishikawa cells were detected by Transwell assay in different groups;They were randomly divided into control group,dexamethasone group,mifepristone group and dexamethasone+mifepristone group and treated with the corresponding drugs,by subcutaneous tumorigenesis of endometrial carcinoma Ishikawa cells in nude mice.GR,Ki67,PCNA and E-cadherin were detected by immunohistochemistry.The expression level of GR,E-cadherin,β-catenin,N-cadherin,vimentin and legumain were detected by Western blot.Result1.The expression of glucocorticoid receptor in endometrial carcinoma was higher than that in normal endometrial tissue(P<0.05).2.The proliferation rate of endometrial cancer cells treated with dexamethasone was increased(P<0.01),and the proliferation rate of endometrial cancer cells treated with mifepristone was significantly decreased(P<0.01).3.The invasion and migration of endometrial cancer cells were enhanced after dexamethasone treatment,but there was no statistical significance;The invasion and migration of endometrial cancer cells were decreased after mifepristone treatment(P<0.01).4.Immunohistochemical results:in dexamethasone treated group,the expression of glucocorticoid receptor,Ki67 and PCNA increased(P<0.05),and the expression of EMT related protein E-cadherin decreased(P<0.05);In mifepristone treated group,the expression of glucocorticoid receptor,Ki67 and PCNA decreased(P<0.05),and the expression of EMT related protein E-cadherin increased(P<0.05),There was no significant difference between dexamethasone+mifepristone group and control group.5.Western blot results:in dexamethasone treated group,the expression of glucocorticoid receptor and β-catenin was increased(P<0.05),and the expression of EMT related protein E-cadherin decreased(P<0.01);in mifepristone treated group,the expression of glucocorticoid receptor and β-catenin was decreased(P<0.05),and the expression of EMT related protein E-cadherin increased(P<0.05);there was no significant difference between dexamethasone+mifepristone group and control group.N-cadherin,Vimentin and Legumain had no statistical significance in each group.Conclusion1.Glucocorticoid receptor was highly expressed in endometrial carcinoma of the study group.2.The high expression of glucocorticoid receptor may be related to the development of endometrial cancer.The high expression of glucocorticoid receptor may promote the development of endometrial cancer,and it may be through Wnt/β-catenin signaling pathway play a role.3.Mifepristone,a glucocorticoid receptor antagonist,has a inhibitory effect on the development of endometrial cancer cell line in vitro,and may play a role by antagonizing glucocorticoids.
Keywords/Search Tags:Endometrial carcinoma, Glucocorticoid receptor, Dexamethasone, Mifepristone, Proliferation, Transfer
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