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10.18632/oncotarget.11927 http://scihub22266oqcxt.onion/10.18632/oncotarget.11927 C5342564!5342564!27626482     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 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 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2016 ; 7 (43): 70447-61 Nephropedia Template TP {{tp|p=27626482|t=2016. A vicious cycle between acid sensing and survival signaling in myeloma cells: acid-induced epigenetic alteration |pdf=|usr=}}{{27626482}} gab.com Text A vicious cycle between acid sensing and survival signaling in myeloma cells: acid-induced epigenetic alteration JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27626482 #FOAvip Myeloma (MM) cells and osteoclasts are mutually interacted to enhance MM growth while creating acidic bone lesions. Here, we explored acid sensing of MM cells and its role in MM cell response to acidic conditions. Acidic conditions activated the PI3K-Akt signaling in MM cells while upregulating the pH sensor transient receptor potential cation channel subfamily V member 1 (TRPV1) in a manner inhibitable by PI3K inhibition. The acid-activated PI3K-Akt signaling facilitated the nuclear localization of the transcription factor Sp1 to trigger the expression of its target genes, including TRPV1 and HDAC1. Consistently, histone deacetylation was enhanced in MM cells in acidic conditions, while repressing a wide variety of genes, including DR4. Indeed, acidic conditions deacetylated histone H3K9 in a DR4 gene promoter and curtailed DR4 expression in MM cells. However, inhibition of HDAC as well as either Sp1 or PI3K was able to restore DR4 expression in MM cells suppressed in acidic conditions. These results collectively demonstrate that acid activates the TRPV1-PI3K-Akt-Sp1 signaling in MM cells while inducing HDAC-mediated gene repression, and suggest that a positive feedback loop between acid sensing and the PI3K-Akt signaling is formed in MM cells, leading to MM cell response to acidic bone lesions. Twit Text FOAVip A vicious cycle between acid sensing and survival signaling in myeloma cells: acid-induced epigenetic alteration ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27626482 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27626482 #FOAvip English Wikipedia <ref>{{Cite pmid|27626482}}</ref> A vicious cycle between acid sensing and survival signaling in myeloma cells: acid-induced epigenetic alteration #MMPMID27626482 Amachi R; Hiasa M; Teramachi J; Harada T; Oda A; Nakamura S; Hanson D; Watanabe K; Fujii S; Miki H; Kagawa K; Iwasa M; Endo I; Kondo T; Yoshida S; Aihara KI; Kurahashi K; Kuroda Y; Horikawa H; Tanaka E; Matsumoto T; Abe M Oncotarget 2016[Oct]; 7 (43): 70447-61 PMID27626482show ga Myeloma (MM) cells and osteoclasts are mutually interacted to enhance MM growth while creating acidic bone lesions. Here, we explored acid sensing of MM cells and its role in MM cell response to acidic conditions. Acidic conditions activated the PI3K-Akt signaling in MM cells while upregulating the pH sensor transient receptor potential cation channel subfamily V member 1 (TRPV1) in a manner inhibitable by PI3K inhibition. The acid-activated PI3K-Akt signaling facilitated the nuclear localization of the transcription factor Sp1 to trigger the expression of its target genes, including TRPV1 and HDAC1. Consistently, histone deacetylation was enhanced in MM cells in acidic conditions, while repressing a wide variety of genes, including DR4. Indeed, acidic conditions deacetylated histone H3K9 in a DR4 gene promoter and curtailed DR4 expression in MM cells. However, inhibition of HDAC as well as either Sp1 or PI3K was able to restore DR4 expression in MM cells suppressed in acidic conditions. These results collectively demonstrate that acid activates the TRPV1-PI3K-Akt-Sp1 signaling in MM cells while inducing HDAC-mediated gene repression, and suggest that a positive feedback loop between acid sensing and the PI3K-Akt signaling is formed in MM cells, leading to MM cell response to acidic bone lesions. äA vicious cycle between acid sensing and survival signaling in myeloma(epmc).pdf DeepDyve Pubget Overpricing