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10.1002/ijc.28919 http://scihub22266oqcxt.onion/10.1002/ijc.28919 C4610361!4610361 !24752651     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24752651 &cmd=llinks): Failed to open stream: HTTP request failed! 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ROBO1, a tumor suppressor and critical molecular barrier for localized tumor cells to acquire invasive phenotype: study in African-American and Caucasian prostate cancer models |pdf=|usr=}}{{24752651 }} gab.com Text ROBO1, a tumor suppressor and critical molecular barrier for localized tumor cells to acquire invasive phenotype: study in African-American and Caucasian prostate cancer models JO: Int J Cancer http://www.kidney.de/pget.php?&tw=1&pmid=24752651 #FOAvip High-risk populations exhibit early transformation of localized prostate cancer (CaP) disease to metastasis which results in the mortality of such patients. The paucity of knowledge about the molecular mechanism involved in acquiring of metastatic behavior by primary tumor cells and non-availability of reliable phenotype-discriminating biomarkers are stumbling blocks in the management of CaP disease. Here, we determine the role and translational relevance of ROBO1 (an organogenesis-associated gene) in human CaP. Employing CaP-progression models and prostatic tissues of Caucasian and African-American patients, we show that ROBO1 expression is localized to cell-membrane and significantly lost in primary and metastatic tumors. While Caucasians exhibited similar ROBO1 levels in primary and metastatic phenotype, a significant difference was observed between tumor phenotypes in African-Americans. Epigenetic assays identified promoter methylation of ROBO1 specific to African-American metastatic CaP cells. Using African-American CaP models for further studies, we show that ROBO1 negatively regulates motility and invasiveness of primary CaP cells, and its loss causes these cells to acquire invasive trait. To understand the underlying mechanism, we employed ROBO1-expressing/ROBO1-C2C3-mutant constructs, immunoprecipitation, confocal-microscopy and luciferase-reporter techniques. We show that ROBO1 through its interaction with DOCK1 (at SH3-SH2-domain) controls the Rac-activation. However, loss of ROBO1 results in Rac1-activation which in turn causes E-Cadherin/?-catenin cytoskeleton destabilization and induction of cell migration. We suggest that ROBO1 is a predictive biomarker that has potential to discriminate among CaP types, and could be exploited as a molecular target to inhibit the progression of disease as well as treat metastasis in high-risk populations such as African-Americans. Twit Text FOAVip ROBO1, a tumor suppressor and critical molecular barrier for localized tumor cells to acquire invasive phenotype: study in African-American and Caucasian prostate cancer models ????Int J Cancer http://www.kidney.de/pget.php?&tw=1&pmid=24752651 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24752651 #FOAvip English Wikipedia <ref>{{Cite pmid|24752651 }}</ref> ROBO1, a tumor suppressor and critical molecular barrier for localized tumor cells to acquire invasive phenotype: study in African-American and Caucasian prostate cancer models #MMPMID24752651 Parray A ; Siddique HR ; Kuriger JK ; Mishra SK ; Rhim JS ; Nelson HH ; Aburatani H ; Konety BR ; Koochekpour S ; Saleem M Int J Cancer 2014[Dec]; 135 (11 ): 2493-506 PMID24752651 show ga High-risk populations exhibit early transformation of localized prostate cancer (CaP) disease to metastasis which results in the mortality of such patients. The paucity of knowledge about the molecular mechanism involved in acquiring of metastatic behavior by primary tumor cells and non-availability of reliable phenotype-discriminating biomarkers are stumbling blocks in the management of CaP disease. Here, we determine the role and translational relevance of ROBO1 (an organogenesis-associated gene) in human CaP. Employing CaP-progression models and prostatic tissues of Caucasian and African-American patients, we show that ROBO1 expression is localized to cell-membrane and significantly lost in primary and metastatic tumors. While Caucasians exhibited similar ROBO1 levels in primary and metastatic phenotype, a significant difference was observed between tumor phenotypes in African-Americans. Epigenetic assays identified promoter methylation of ROBO1 specific to African-American metastatic CaP cells. Using African-American CaP models for further studies, we show that ROBO1 negatively regulates motility and invasiveness of primary CaP cells, and its loss causes these cells to acquire invasive trait. To understand the underlying mechanism, we employed ROBO1-expressing/ROBO1-C2C3-mutant constructs, immunoprecipitation, confocal-microscopy and luciferase-reporter techniques. We show that ROBO1 through its interaction with DOCK1 (at SH3-SH2-domain) controls the Rac-activation. However, loss of ROBO1 results in Rac1-activation which in turn causes E-Cadherin/?-catenin cytoskeleton destabilization and induction of cell migration. We suggest that ROBO1 is a predictive biomarker that has potential to discriminate among CaP types, and could be exploited as a molecular target to inhibit the progression of disease as well as treat metastasis in high-risk populations such as African-Americans. |*Genes, Tumor Suppressor [MESH] |Black or African American/*statistics & numerical data [MESH] |Blotting, Western [MESH] |Cadherins/genetics/metabolism [MESH] |Cell Movement [MESH] |Cell Proliferation [MESH] |Cohort Studies [MESH] |Disease Progression [MESH] |Fluorescent Antibody Technique [MESH] |Gene Expression Regulation, Neoplastic [MESH] |Humans [MESH] |Immunoenzyme Techniques [MESH] |Male [MESH] |Neoplasm Metastasis [MESH] |Neoplasm Staging [MESH] |Nerve Tissue Proteins/antagonists & inhibitors/genetics/*metabolism [MESH] |Phenotype [MESH] |Promoter Regions, Genetic/genetics [MESH] |Prostatic Neoplasms/*ethnology/metabolism/*pathology [MESH] |RNA, Messenger/genetics [MESH] |RNA, Small Interfering/genetics [MESH] |Real-Time Polymerase Chain Reaction [MESH] |Receptors, Immunologic/antagonists & inhibitors/genetics/*metabolism [MESH] |Reverse Transcriptase Polymerase Chain Reaction [MESH] |Roundabout Proteins [MESH] |Tumor Cells, Cultured [MESH] |White People/*statistics & numerical data [MESH] |Wound Healing [MESH] |beta Catenin/genetics/metabolism [MESH] |rac GTP-Binding Proteins/genetics/metabolism [MESH]ROBO1, a tumor suppressor and critical molecular barrier for localized(epmc).pdf DeepDyve Pubget Overpricing