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10.2147/OTT.S90085 http://scihub22266oqcxt.onion/10.2147/OTT.S90085 C4608546!4608546 !26491358     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26491358 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Onco+Targets+Ther 2015 ; 8 (ä): 2849-63 Nephropedia Template TP {{tp|p=26491358 |t=2015. Role of estrogen in lung cancer based on the estrogen receptor-epithelial mesenchymal transduction signaling pathways |pdf=|usr=}}{{26491358 }} gab.com Text Role of estrogen in lung cancer based on the estrogen receptor-epithelial mesenchymal transduction signaling pathways JO: Onco Targets Ther http://www.kidney.de/pget.php?&tw=1&pmid=26491358 #FOAvip BACKGROUND/AIM: Estrogen is reported to promote the occurrence and development of several human cancers. Increasing evidence shows that most human lung tumors exert estrogen receptor expression. In the present study, we investigated the underlying mechanism of estrogen effect in lung cancer through estrogen receptor-epithelial-mesechymal-transition signaling pathways for the first time. MATERIALS AND METHODS: A total of 36 inbred C57BL/6 mice (18 male and 18 female) were injected subcutaneously with human lung adenocarcinoma cell line, Lewis. After the lung tumor model was established, mice with lung adenocarcinoma were randomly divided into three groups for each sex (n=6), such as vehicle group, estrogen group, and estrogen plus tamoxifen group. The six groups of mice were sacrificed after 21 days of drug treatment. Tumor tissue was stripped and weighed, and tumor inhibition rate was calculated based on average tumor weight. Protein and messenger RNA (mRNA) expressions of estrogen receptor ? (ER?), estrogen receptor ? (ER?), phosphatidylinositol 3'-kinase (PI3K), AKT, E-cadherin, and vimentin were detected in both tumor tissue and lung tissue by using immunohistochemistry and real-time reverse transcription-polymerase chain reaction. RESULTS: 1) For male mice: in the estrogen group, estrogen treatment significantly increased ER? protein and mRNA expressions in tumor tissue and protein expression of PI3K, AKT, and vimentin in both tumor tissue and lung tissue compared with the vehicle-treated group. Besides, mRNA expression of E-cadherin was significantly reduced in estrogen-treated tumor tissues than that in vehicle-treated tissues. In the estrogen plus tamoxifen group, protein and mRNA expressions of ER? and AKT were dramatically reduced by tamoxifen treatment in tumor tissue compared with the estrogen group; mRNA expression of E-cadherin was increased in tumor tissue; protein expression of vimentin and PI3K were downregulated in tumor tissue; protein expression of E-cadherin increased in lung tissue; protein expression of ER? and PI3K were downregulated in lung tissue compared with the estrogen group. 2) For female mice: in the estrogen group, estrogen treatment significantly increased mRNA expression of ER? and PI3K, and protein expression of ER?, PI3K, AKT, and vimentin in both tumor tissue and lung tissue compared with the vehicle-treated group. mRNA expression of E-cadherin was downregulated in tumor tissue, and mRNA expression of AKT was increased in lung tissues compared with the vehicle-treated group. In the estrogen plus tamoxifen group, tamoxifen treatment dramatically reduced protein expression of ER?, ER?, AKT, and vimentin but significantly increased protein expression of E-cadherin in tumor tissues and lung tissue compared with the estrogen group. mRNA expression of ER?, PI3K, and AKT was dramatically reduced by tamoxifen treatment in lung tissues compared with the estrogen group. CONCLUSION: Estrogen promoted lung adenocarcinoma cell metastasis by inducing lung epithelial mesenchymal cells and reducing intercellular adhesion force through PI3K/AKT signaling pathway. Twit Text FOAVip Role of estrogen in lung cancer based on the estrogen receptor-epithelial mesenchymal transduction signaling pathways ????Onco Targets Ther http://www.kidney.de/pget.php?&tw=1&pmid=26491358 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26491358 #FOAvip English Wikipedia <ref>{{Cite pmid|26491358 }}</ref> Role of estrogen in lung cancer based on the estrogen receptor-epithelial mesenchymal transduction signaling pathways #MMPMID26491358 Zhao XZ ; Liu Y ; Zhou LJ ; Wang ZQ ; Wu ZH ; Yang XY Onco Targets Ther 2015[]; 8 (ä): 2849-63 PMID26491358 show ga BACKGROUND/AIM: Estrogen is reported to promote the occurrence and development of several human cancers. Increasing evidence shows that most human lung tumors exert estrogen receptor expression. In the present study, we investigated the underlying mechanism of estrogen effect in lung cancer through estrogen receptor-epithelial-mesechymal-transition signaling pathways for the first time. MATERIALS AND METHODS: A total of 36 inbred C57BL/6 mice (18 male and 18 female) were injected subcutaneously with human lung adenocarcinoma cell line, Lewis. After the lung tumor model was established, mice with lung adenocarcinoma were randomly divided into three groups for each sex (n=6), such as vehicle group, estrogen group, and estrogen plus tamoxifen group. The six groups of mice were sacrificed after 21 days of drug treatment. Tumor tissue was stripped and weighed, and tumor inhibition rate was calculated based on average tumor weight. Protein and messenger RNA (mRNA) expressions of estrogen receptor ? (ER?), estrogen receptor ? (ER?), phosphatidylinositol 3'-kinase (PI3K), AKT, E-cadherin, and vimentin were detected in both tumor tissue and lung tissue by using immunohistochemistry and real-time reverse transcription-polymerase chain reaction. RESULTS: 1) For male mice: in the estrogen group, estrogen treatment significantly increased ER? protein and mRNA expressions in tumor tissue and protein expression of PI3K, AKT, and vimentin in both tumor tissue and lung tissue compared with the vehicle-treated group. Besides, mRNA expression of E-cadherin was significantly reduced in estrogen-treated tumor tissues than that in vehicle-treated tissues. In the estrogen plus tamoxifen group, protein and mRNA expressions of ER? and AKT were dramatically reduced by tamoxifen treatment in tumor tissue compared with the estrogen group; mRNA expression of E-cadherin was increased in tumor tissue; protein expression of vimentin and PI3K were downregulated in tumor tissue; protein expression of E-cadherin increased in lung tissue; protein expression of ER? and PI3K were downregulated in lung tissue compared with the estrogen group. 2) For female mice: in the estrogen group, estrogen treatment significantly increased mRNA expression of ER? and PI3K, and protein expression of ER?, PI3K, AKT, and vimentin in both tumor tissue and lung tissue compared with the vehicle-treated group. mRNA expression of E-cadherin was downregulated in tumor tissue, and mRNA expression of AKT was increased in lung tissues compared with the vehicle-treated group. In the estrogen plus tamoxifen group, tamoxifen treatment dramatically reduced protein expression of ER?, ER?, AKT, and vimentin but significantly increased protein expression of E-cadherin in tumor tissues and lung tissue compared with the estrogen group. mRNA expression of ER?, PI3K, and AKT was dramatically reduced by tamoxifen treatment in lung tissues compared with the estrogen group. CONCLUSION: Estrogen promoted lung adenocarcinoma cell metastasis by inducing lung epithelial mesenchymal cells and reducing intercellular adhesion force through PI3K/AKT signaling pathway. äRole of estrogen in lung cancer based on the estrogen receptor-epithel(epmc).pdf DeepDyve Pubget Overpricing