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10.18632/oncotarget.11909 http://scihub22266oqcxt.onion/10.18632/oncotarget.11909 C5340126!5340126!27626309     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       Oncotarget 2016 ; 7 (45): 72777-94 Nephropedia Template TP {{tp|p=27626309|t=2016. c-Abl inhibits breast cancer tumorigenesis through reactivation of p53-mediated p21 expression |pdf=|usr=}}{{27626309}} gab.com Text c-Abl inhibits breast cancer tumorigenesis through reactivation of p53-mediated p21 expression JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27626309 #FOAvip We previously reported that constitutive c-Abl activity (CST-Abl) abrogates the tumorigenicity of triple-negative breast cancer cells through the combined actions of two cellular events: downregulated matrix metalloproteinase (MMP) and upregulated p21Waf1/Cip1 expression. We now find decreased c-Abl expression to be significantly associated with diminished relapse-fee survival in breast cancer patients, particularly those exhibiting invasive and basal phenotypes. Moreover, CST-Abl expression enabled 4T1 cells to persist innocuously in the mammary glands of mice, doing so by exhausting their supply of cancer stem cells. Restoring MMP-9 expression and activity in CST-Abl-expressing 4T1 cells failed to rescue their malignant phenotypes; however, rendering these same cells deficient in p21 expression not only delayed their acquisition of senescent phenotypes, but also partially restored their tumorigenicity in mice. Although 4T1 cells lacked detectable expression of p53, those engineered to express CST-Abl exhibited robust production and secretion of TGF-?1 that engendered the reactivated expression of p53. Mechanistically, TGF-?-mediated p53 expression transpired through the combined actions of Smad1/5/8 and Smad2, leading to the dramatic upregulation of p21 and its stimulation of TNBC senescence. Collectively, we identified a novel c-Abl:p53:p21 signaling axis that functions as a powerful suppressor of mammary tumorigenesis and metastatic progression. Twit Text FOAVip c-Abl inhibits breast cancer tumorigenesis through reactivation of p53-mediated p21 expression ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27626309 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27626309 #FOAvip English Wikipedia <ref>{{Cite pmid|27626309}}</ref> c-Abl inhibits breast cancer tumorigenesis through reactivation of p53-mediated p21 expression #MMPMID27626309 Morrison CD; Allington TM; Thompson CL; Gilmore HL; Chang JC; Keri RA; Schiemann WP Oncotarget 2016[Nov]; 7 (45): 72777-94 PMID27626309show ga We previously reported that constitutive c-Abl activity (CST-Abl) abrogates the tumorigenicity of triple-negative breast cancer cells through the combined actions of two cellular events: downregulated matrix metalloproteinase (MMP) and upregulated p21Waf1/Cip1 expression. We now find decreased c-Abl expression to be significantly associated with diminished relapse-fee survival in breast cancer patients, particularly those exhibiting invasive and basal phenotypes. Moreover, CST-Abl expression enabled 4T1 cells to persist innocuously in the mammary glands of mice, doing so by exhausting their supply of cancer stem cells. Restoring MMP-9 expression and activity in CST-Abl-expressing 4T1 cells failed to rescue their malignant phenotypes; however, rendering these same cells deficient in p21 expression not only delayed their acquisition of senescent phenotypes, but also partially restored their tumorigenicity in mice. Although 4T1 cells lacked detectable expression of p53, those engineered to express CST-Abl exhibited robust production and secretion of TGF-?1 that engendered the reactivated expression of p53. Mechanistically, TGF-?-mediated p53 expression transpired through the combined actions of Smad1/5/8 and Smad2, leading to the dramatic upregulation of p21 and its stimulation of TNBC senescence. Collectively, we identified a novel c-Abl:p53:p21 signaling axis that functions as a powerful suppressor of mammary tumorigenesis and metastatic progression. äc-Abl inhibits breast cancer tumorigenesis through reactivation of p53(epmc).pdf DeepDyve Pubget Overpricing