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10.1038/bjc.2014.141 http://scihub22266oqcxt.onion/10.1038/bjc.2014.141 C3992501!3992501 !24642616     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24642616 &cmd=llinks): Failed to open stream: HTTP request failed! 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Restoration of PPP2CA expression reverses epithelial-to-mesenchymal transition and suppresses prostate tumour growth and metastasis in an orthotopic mouse model |pdf=|usr=}}{{24642616 }} gab.com Text Restoration of PPP2CA expression reverses epithelial-to-mesenchymal transition and suppresses prostate tumour growth and metastasis in an orthotopic mouse model JO: Br J Cancer http://www.kidney.de/pget.php?&tw=1&pmid=24642616 #FOAvip BACKGROUND: Emergence of castration-resistance in prostate cancer (PCa) is invariably associated with aggressive and metastatic disease. Previously, we reported promotion of castration-resistance upon downregulation of PPP2CA (encoding catalytic subunit of protein phosphatase 2A (PP2A), ?-isoform); however, its role in PCa growth and metastasis remained undetermined. METHODS: PPP2CA was overexpressed/silenced in PCa cells by stable transfection. Gene expression was examined by reverse transcription polymerase chain reaction, immunoblot and immunofluorescence analyses, and transcriptional activity measured by luciferase-based promoter-reporter assay. Effect on PCa phenotype was studied in vitro and in orthotopic mouse model, and immunohistochemical/histological analyses performed to assess proliferation/apoptosis and confirm metastatic lesions. RESULTS: An inverse association of PPP2CA expression was observed with epithelial-to-mesenchymal transition (EMT) and aggressive PCa phenotype. PPP2CA restoration resulted in decreased nuclear accumulation and transcriptional activity of ?-catenin/NF-?B, and restitution of their activity abrogated PPP2CA-induced EMT reversal and suppression of PCa invasiveness. Akt mediated PPP2CA loss-induced nuclear accumulation of ?-catenin/NF-?B through inactivation of Gsk3-? and I?B-?, respectively. Animal studies revealed a suppressive effect of PPP2CA expression on PCa growth and metastasis. CONCLUSIONS: Our findings suggest that PPP2CA downregulation serves as a molecular link between gain of castration-resistance and aggressive PCa phenotype, and its restoration could be an effective preventive/therapeutic approach against the advanced disease. Twit Text FOAVip Restoration of PPP2CA expression reverses epithelial-to-mesenchymal transition and suppresses prostate tumour growth and metastasis in an orthotopic mouse model ????Br J Cancer http://www.kidney.de/pget.php?&tw=1&pmid=24642616 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24642616 #FOAvip English Wikipedia <ref>{{Cite pmid|24642616 }}</ref> Restoration of PPP2CA expression reverses epithelial-to-mesenchymal transition and suppresses prostate tumour growth and metastasis in an orthotopic mouse model #MMPMID24642616 Bhardwaj A ; Singh S ; Srivastava SK ; Arora S ; Hyde SJ ; Andrews J ; Grizzle WE ; Singh AP Br J Cancer 2014[Apr]; 110 (8 ): 2000-10 PMID24642616 show ga BACKGROUND: Emergence of castration-resistance in prostate cancer (PCa) is invariably associated with aggressive and metastatic disease. Previously, we reported promotion of castration-resistance upon downregulation of PPP2CA (encoding catalytic subunit of protein phosphatase 2A (PP2A), ?-isoform); however, its role in PCa growth and metastasis remained undetermined. METHODS: PPP2CA was overexpressed/silenced in PCa cells by stable transfection. Gene expression was examined by reverse transcription polymerase chain reaction, immunoblot and immunofluorescence analyses, and transcriptional activity measured by luciferase-based promoter-reporter assay. Effect on PCa phenotype was studied in vitro and in orthotopic mouse model, and immunohistochemical/histological analyses performed to assess proliferation/apoptosis and confirm metastatic lesions. RESULTS: An inverse association of PPP2CA expression was observed with epithelial-to-mesenchymal transition (EMT) and aggressive PCa phenotype. PPP2CA restoration resulted in decreased nuclear accumulation and transcriptional activity of ?-catenin/NF-?B, and restitution of their activity abrogated PPP2CA-induced EMT reversal and suppression of PCa invasiveness. Akt mediated PPP2CA loss-induced nuclear accumulation of ?-catenin/NF-?B through inactivation of Gsk3-? and I?B-?, respectively. Animal studies revealed a suppressive effect of PPP2CA expression on PCa growth and metastasis. CONCLUSIONS: Our findings suggest that PPP2CA downregulation serves as a molecular link between gain of castration-resistance and aggressive PCa phenotype, and its restoration could be an effective preventive/therapeutic approach against the advanced disease. |*Molecular Targeted Therapy [MESH] |Animals [MESH] |Disease Models, Animal [MESH] |Epithelial-Mesenchymal Transition/*genetics [MESH] |Gene Expression Regulation, Neoplastic [MESH] |Gene Knockdown Techniques [MESH] |Humans [MESH] |Male [MESH] |Mice [MESH] |Neoplasm Metastasis/genetics/pathology [MESH] |Prostatic Neoplasms, Castration-Resistant/drug therapy/*genetics/pathology [MESH] |Protein Phosphatase 2/antagonists & inhibitors/biosynthesis/*genetics [MESH]Restoration of PPP2CA expression reverses epithelial-to-mesenchymal tr(epmc).pdf DeepDyve Pubget Overpricing