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《Chongqing Medicine》 2017-05
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Study on the role of GPR30 in the proliferation of Non-small cell lung cancer

Ruan Shuqin;Huang Wei;Yang Zhixiang;Wei Feng;Tang Min;Department of Oncology and Hematology,Chongqing General Hospital;Department of Thoracic Surgery,Chongqing General Hospital;  
Objective To evaluate the expression of GPR30 and Ki-67 in Non-small cell lung cancer(NSCLC)and the relationship between them.The clinicopathological features of GPR30 in NSCLC were also analyzed.The molecular mechanism that estrogen mediated the proliferation of H1299 by activating GPR30 was further studied.Methods The expression of GPR30 and Ki-67 in 80cases of specimens of NSCLC after surgery was examined using immunohistochemistry method.After 17-β-estradiol(E2)or G-1added,H1299 cells were counted and the cell cycle distribution was analyzed by flow cytometry.Finally,the activated ERK1/2and the expression of cyclin D1 and p16after G-1treatment in H1299 cells were examined through western blotting.Results Expressions of GPR30 was more in stageⅢ or low differentiation tissues or adenocarcinoma(P0.05).A positive correlation between GPR30 and Ki-67 was further disclosed(r=0.502,P=0.000).The proliferation of H1299 cells was promoted and more cells entered S-phase after E2 or G-1treatment for 3days,which could be inhibited after G-15 or U0126pre-treatment for 2hours.We further discovered that the activated ERK1/2and cyclin D1 expression increased after G-1treatment,which was blocked after G-15 or U0126pre-treatment for 2hours.The change of p16 was on the opposite.Conclusion A positive correlation existed between GPR30 and Ki-67.GPR30-EGFR-MAPKs signaling transduction pathway was involved in the estrogen-induced proliferation of NSCLC cells.Blocking GPR30 signaling pathway may be a promising new strategy for NSCLC treatments.
【Fund】: 重庆市卫生局医学科研项目(2013-2-111);; 重庆市渝中区科技计划项目(20130144)
【CateGory Index】: R734.2
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