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10.1002/1878-0261.12059 http://scihub22266oqcxt.onion/10.1002/1878-0261.12059 C5467496!5467496!28371345     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       Mol+Oncol 2017 ; 11 (6): 655-69 Nephropedia Template TP {{tp|p=28371345|t=2017. The prostate metastasis suppressor gene NDRG1 differentially regulates cell motility and invasion |pdf=|usr=}}{{28371345}} gab.com Text The prostate metastasis suppressor gene NDRG1 differentially regulates cell motility and invasion JO: Mol Oncol http://www.kidney.de/pget.php?&tw=1&pmid=28371345 #FOAvip Experimental and clinical evidence suggests that N?myc downregulated gene 1 (NDRG1) functions as a suppressor of prostate cancer metastasis. Elucidating pathways that drive survival and invasiveness of NDRG1?deficient prostate cancer cells can help in designing therapeutics to target metastatic prostate cancer cells. However, the molecular mechanisms that lead NDRG1?deficient prostate cancer cells to increased invasiveness remain largely unknown. In this study, we demonstrate that NDRG1?deficient prostate tumors have decreased integrin expression and reduced cell adhesion and motility. Our data indicate that loss of NDRG1 differentially affects Rho GTPases. Specifically, there is a downregulation of active RhoA and Rac1 GTPases with a concomitant upregulation of active Cdc42 in NDRG1?deficient cells. Live cell imaging using a fluorescent sensor that binds to polymerized actin revealed that NDRG1?deficient cells have restricted actin dynamics, thereby affecting cell migration. These cellular and molecular characteristics are in sharp contrast to what is expected after loss of a metastasis suppressor. We further demonstrate that NDRG1?deficient cells have increased resistance to anoikis and increased invasiveness which is independent of its elevated Cdc42 activity. Furthermore, NDRG1 regulates expression and glycosylation of EMMPRIN, a master regulator of matrix metalloproteases. NDRG1 deficiency leads to an increase in EMMPRIN expression with a concomitant increase in matrix metalloproteases and thus invadopodial activity. Using a three?dimensional invasion assay and an in vivo metastasis assay for human prostate xenografts, we demonstrate that NDRG1?deficient prostate cancer cells exhibit a collective invasion phenotype and are highly invasive. Thus, our findings provide novel insights suggesting that loss of NDRG1 leads to a decrease in actin?mediated cellular motility but an increase in cellular invasion, resulting in increased tumor dissemination which positively impacts metastatic outcome. Twit Text FOAVip The prostate metastasis suppressor gene NDRG1 differentially regulates cell motility and invasion ????Mol Oncol http://www.kidney.de/pget.php?&tw=1&pmid=28371345 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28371345 #FOAvip English Wikipedia <ref>{{Cite pmid|28371345}}</ref> The prostate metastasis suppressor gene NDRG1 differentially regulates cell motility and invasion #MMPMID28371345 Sharma A; Mendonca J; Ying J; Kim H; Verdone JE; Zarif JC; Carducci M; Hammers H; Pienta KJ; Kachhap S Mol Oncol 2017[Jun]; 11 (6): 655-69 PMID28371345show ga Experimental and clinical evidence suggests that N?myc downregulated gene 1 (NDRG1) functions as a suppressor of prostate cancer metastasis. Elucidating pathways that drive survival and invasiveness of NDRG1?deficient prostate cancer cells can help in designing therapeutics to target metastatic prostate cancer cells. However, the molecular mechanisms that lead NDRG1?deficient prostate cancer cells to increased invasiveness remain largely unknown. In this study, we demonstrate that NDRG1?deficient prostate tumors have decreased integrin expression and reduced cell adhesion and motility. Our data indicate that loss of NDRG1 differentially affects Rho GTPases. Specifically, there is a downregulation of active RhoA and Rac1 GTPases with a concomitant upregulation of active Cdc42 in NDRG1?deficient cells. Live cell imaging using a fluorescent sensor that binds to polymerized actin revealed that NDRG1?deficient cells have restricted actin dynamics, thereby affecting cell migration. These cellular and molecular characteristics are in sharp contrast to what is expected after loss of a metastasis suppressor. We further demonstrate that NDRG1?deficient cells have increased resistance to anoikis and increased invasiveness which is independent of its elevated Cdc42 activity. Furthermore, NDRG1 regulates expression and glycosylation of EMMPRIN, a master regulator of matrix metalloproteases. NDRG1 deficiency leads to an increase in EMMPRIN expression with a concomitant increase in matrix metalloproteases and thus invadopodial activity. Using a three?dimensional invasion assay and an in vivo metastasis assay for human prostate xenografts, we demonstrate that NDRG1?deficient prostate cancer cells exhibit a collective invasion phenotype and are highly invasive. Thus, our findings provide novel insights suggesting that loss of NDRG1 leads to a decrease in actin?mediated cellular motility but an increase in cellular invasion, resulting in increased tumor dissemination which positively impacts metastatic outcome. äThe prostate metastasis suppressor gene NDRG1 differentially regulates(epmc).pdf DeepDyve Pubget Overpricing