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10.18632/oncotarget.17674 http://scihub22266oqcxt.onion/10.18632/oncotarget.17674 C5581085!5581085!28881786     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2017 ; 8 (32): 52960-74 Nephropedia Template TP {{tp|p=28881786|t=2017. TUSC3 induces autophagy in human non-small cell lung cancer cells through Wnt/?-catenin signaling |pdf=|usr=}}{{28881786}} gab.com Text TUSC3 induces autophagy in human non-small cell lung cancer cells through Wnt/ -catenin signaling JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28881786 #FOAvip We investigated the effects of tumor suppressor candidate 3 (TUSC3) on autophagy in human non-small cell lung cancer (NSCLC) cells. A total of 118 NSCLC patients (88 males and 30 females) who underwent surgery at our institute were enrolled in the study. Immunohistochemical analysis revealed that TUSC3 protein expression was lower in NSCLC specimens than adjacent normal tissue. Correspondingly, there was greater methylation of TUSC3 in NSCLC than adjacent normal tissue. After transient transfection of A549 NSCLC cells with constructs designed to up-regulate or down-regulate TUSC3 expression, we analyzed the effects of inhibiting the Wnt pathway (XAV939) and autophagy (chloroquine, CQ) on the behavior of NSCLC cells. We also performed TOP/FOP-Flash reporter assays, MTT assays, Annexin V-FITC/propidium iodide staining, and acridine orange staining to evaluate Wnt/?-catenin signaling, cell proliferation, apoptosis, and autophagy, respectively. Expression of Wnt/?-catenin pathway components and autophagy-related proteins was analyzed using qRT-PCR and Western blotting. We found that TUSC3 inhibited cell proliferation and promoted both apoptosis and autophagy in A549 cells. In addition, TUSC3 increased expression of autophagy-related proteins. It also increased expression of Wnt/?-catenin signaling pathway components and promoted nuclear transfer of ?-catenin, resulting in activation of Wnt/?-catenin signaling. TUSC3 thus induces autophagy in human NSCLC cells through activation of the Wnt/?-catenin signaling pathway. Twit Text FOAVip TUSC3 induces autophagy in human non-small cell lung cancer cells through Wnt/ -catenin signaling ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28881786 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28881786 #FOAvip English Wikipedia <ref>{{Cite pmid|28881786}}</ref> TUSC3 induces autophagy in human non-small cell lung cancer cells through Wnt/?-catenin signaling #MMPMID28881786 Peng Y; Cao J; Yao XY; Wang JX; Zhong MZ; Gan PP; Li JH Oncotarget 2017[Aug]; 8 (32): 52960-74 PMID28881786show ga We investigated the effects of tumor suppressor candidate 3 (TUSC3) on autophagy in human non-small cell lung cancer (NSCLC) cells. A total of 118 NSCLC patients (88 males and 30 females) who underwent surgery at our institute were enrolled in the study. Immunohistochemical analysis revealed that TUSC3 protein expression was lower in NSCLC specimens than adjacent normal tissue. Correspondingly, there was greater methylation of TUSC3 in NSCLC than adjacent normal tissue. After transient transfection of A549 NSCLC cells with constructs designed to up-regulate or down-regulate TUSC3 expression, we analyzed the effects of inhibiting the Wnt pathway (XAV939) and autophagy (chloroquine, CQ) on the behavior of NSCLC cells. We also performed TOP/FOP-Flash reporter assays, MTT assays, Annexin V-FITC/propidium iodide staining, and acridine orange staining to evaluate Wnt/?-catenin signaling, cell proliferation, apoptosis, and autophagy, respectively. Expression of Wnt/?-catenin pathway components and autophagy-related proteins was analyzed using qRT-PCR and Western blotting. We found that TUSC3 inhibited cell proliferation and promoted both apoptosis and autophagy in A549 cells. In addition, TUSC3 increased expression of autophagy-related proteins. It also increased expression of Wnt/?-catenin signaling pathway components and promoted nuclear transfer of ?-catenin, resulting in activation of Wnt/?-catenin signaling. TUSC3 thus induces autophagy in human NSCLC cells through activation of the Wnt/?-catenin signaling pathway. äTUSC3 induces autophagy in human non-small cell lung cancer cells thro(epmc).pdf DeepDyve Pubget Overpricing