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10.1186/s12943-015-0414-1 http://scihub22266oqcxt.onion/10.1186/s12943-015-0414-1 C4518688!4518688!26223682     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Cancer 2015 ; 14 (ä): ä Nephropedia Template TP {{tp|p=26223682|t=2015. Stratifin accelerates progression of lung adenocarcinoma at an early stage |pdf=|usr=}}{{26223682}} gab.com Text Stratifin accelerates progression of lung adenocarcinoma at an early stage JO: Mol Cancer http://www.kidney.de/pget.php?&tw=1&pmid=26223682 #FOAvip Backgrounds: Adenocarcinoma in situ (AIS) of the lung has an extremely favorable prognosis. However, early but invasive adenocarcinoma (eIA) sometimes has a fatal outcome. We had previously compared the expression profiles of AIS with those of eIA showing lymph node metastasis or a fatal outcome, and found that stratifin (SFN, 14-3-3 sigma) was a differentially expressed gene related to cell proliferation. Here, we performed an in vivo study to clarify the role of SFN in initiation and progression of lung adenocarcinoma. Findings: Suppression of SFN expression in A549 (a human lung adenocarcinoma cell line) by siSFN significantly reduced cell proliferation activity and the S-phase subpopulation. In vivo, tumor development or metastasis to the lung was reduced in shSFN-transfected A549 cells. Moreover, we generated SFN-transgenic mice (Tg-SPC-SFN+/?) showing lung-specific expression of human SFN under the control of a tissue-specific enhancer, the SPC promoter. We found that Tg-SPC-SFN+/? mice developed lung tumors at a significantly higher rate than control mice after administration of chemical carcinogen, NNK. Interestingly, several Tg-SPC-SFN+/? mice developed tumors without NNK. These tumor cells showed high hSFN expression. Conclusion: These results suggest that SFN facilitates lung tumor development and progression. SFN appears to be a novel oncogene with potential as a therapeutic target. Electronic supplementary material: The online version of this article (doi:10.1186/s12943-015-0414-1) contains supplementary material, which is available to authorized users. Twit Text FOAVip Stratifin accelerates progression of lung adenocarcinoma at an early stage ????Mol Cancer http://www.kidney.de/pget.php?&tw=1&pmid=26223682 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26223682 #FOAvip English Wikipedia <ref>{{Cite pmid|26223682}}</ref> Stratifin accelerates progression of lung adenocarcinoma at an early stage #MMPMID26223682 Shiba-Ishii A; Kim Y; Shiozawa T; Iyama S; Satomi K; Kano J; Sakashita S; Morishita Y; Noguchi M Mol Cancer 2015[]; 14 (ä): ä PMID26223682show ga Backgrounds: Adenocarcinoma in situ (AIS) of the lung has an extremely favorable prognosis. However, early but invasive adenocarcinoma (eIA) sometimes has a fatal outcome. We had previously compared the expression profiles of AIS with those of eIA showing lymph node metastasis or a fatal outcome, and found that stratifin (SFN, 14-3-3 sigma) was a differentially expressed gene related to cell proliferation. Here, we performed an in vivo study to clarify the role of SFN in initiation and progression of lung adenocarcinoma. Findings: Suppression of SFN expression in A549 (a human lung adenocarcinoma cell line) by siSFN significantly reduced cell proliferation activity and the S-phase subpopulation. In vivo, tumor development or metastasis to the lung was reduced in shSFN-transfected A549 cells. Moreover, we generated SFN-transgenic mice (Tg-SPC-SFN+/?) showing lung-specific expression of human SFN under the control of a tissue-specific enhancer, the SPC promoter. We found that Tg-SPC-SFN+/? mice developed lung tumors at a significantly higher rate than control mice after administration of chemical carcinogen, NNK. Interestingly, several Tg-SPC-SFN+/? mice developed tumors without NNK. These tumor cells showed high hSFN expression. Conclusion: These results suggest that SFN facilitates lung tumor development and progression. SFN appears to be a novel oncogene with potential as a therapeutic target. Electronic supplementary material: The online version of this article (doi:10.1186/s12943-015-0414-1) contains supplementary material, which is available to authorized users. äStratifin accelerates progression of lung adenocarcinoma at an early s(epmc).pdf DeepDyve Pubget Overpricing