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10.1186/s12885-017-3616-7 http://scihub22266oqcxt.onion/10.1186/s12885-017-3616-7 C5602878!5602878!28915803     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28915803&cmd=llinks): Failed to open stream: HTTP request failed! 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Tartrate-resistant acid phosphatase (TRAP/ACP5) promotes metastasis-related properties via TGF?2/T?R and CD44 in MDA-MB-231 breast cancer cells |pdf=|usr=}}{{28915803}} gab.com Text Tartrate-resistant acid phosphatase (TRAP/ACP5) promotes metastasis-related properties via TGF 2/T R and CD44 in MDA-MB-231 breast cancer cells JO: BMC Cancer http://www.kidney.de/pget.php?&tw=1&pmid=28915803 #FOAvip Background: Tartrate-resistant acid phosphatase (TRAP/ACP5), a metalloenzyme that is characteristic for its expression in activated osteoclasts and in macrophages, has recently gained considerable focus as a driver of metastasis and was associated with clinically relevant parameters of cancer progression and cancer aggressiveness. Methods: MDA-MB-231 breast cancer cells with different TRAP expression levels (overexpression and knockdown) were generated and characterized for protein expression and activity levels. Functional cell experiments, such as proliferation, migration and invasion assays were performed as well as global phosphoproteomic and proteomic analysis was conducted to connect molecular perturbations to the phenotypic changes. Results: We identified an association between metastasis-related properties of TRAP-overexpressing MDA-MB-231 breast cancer cells and a TRAP-dependent regulation of Transforming growth factor (TGF?) pathway proteins and Cluster of differentiation 44 (CD44). Overexpression of TRAP increased anchorage-independent and anchorage-dependent cell growth and proliferation, induced a more elongated cellular morphology and promoted cell migration and invasion. Migration was increased in the presence of the extracellular matrix (ECM) proteins osteopontin and fibronectin and the basement membrane proteins collagen IV and laminin I. TRAP-induced properties were reverted upon shRNA-mediated knockdown of TRAP or treatment with the small molecule TRAP inhibitor 5-PNA. Global phosphoproteomics and proteomics analyses identified possible substrates of TRAP phosphatase activity or signaling intermediates and outlined a TRAP-dependent regulation of proteins involved in cell adhesion and ECM organization. Upregulation of TGF? isoform 2 (TGF?2), TGF? receptor type 1 (T?R1) and Mothers against decapentaplegic homolog 2 (SMAD2), as well as increased intracellular phosphorylation of CD44 were identified upon TRAP perturbation. Functional antibody-mediated blocking and chemical inhibition demonstrated that TRAP-dependent migration and proliferation is regulated via TGF?2/T?R, whereas proliferation beyond basal levels is regulated through CD44. Conclusion: Altogether, TRAP promotes metastasis-related cell properties in MDA-MB-231 breast cancer cells via TGF?2/T?R and CD44, thereby identifying a potential signaling mechanism associated to TRAP action in breast cancer cells. Electronic supplementary material: The online version of this article doi:(10.1186/s12885-017-3616-7) contains supplementary material, which is available to authorized users. Twit Text FOAVip Tartrate-resistant acid phosphatase (TRAP/ACP5) promotes metastasis-related properties via TGF 2/T R and CD44 in MDA-MB-231 breast cancer cells ????BMC Cancer http://www.kidney.de/pget.php?&tw=1&pmid=28915803 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28915803 #FOAvip English Wikipedia <ref>{{Cite pmid|28915803}}</ref> Tartrate-resistant acid phosphatase (TRAP/ACP5) promotes metastasis-related properties via TGF?2/T?R and CD44 in MDA-MB-231 breast cancer cells #MMPMID28915803 Reithmeier A; Panizza E; Krumpel M; Orre LM; Branca RMM; Lehtiö J; Ek-Rylander B; Andersson G BMC Cancer 2017[]; 17 (ä): ä PMID28915803show ga Background: Tartrate-resistant acid phosphatase (TRAP/ACP5), a metalloenzyme that is characteristic for its expression in activated osteoclasts and in macrophages, has recently gained considerable focus as a driver of metastasis and was associated with clinically relevant parameters of cancer progression and cancer aggressiveness. Methods: MDA-MB-231 breast cancer cells with different TRAP expression levels (overexpression and knockdown) were generated and characterized for protein expression and activity levels. Functional cell experiments, such as proliferation, migration and invasion assays were performed as well as global phosphoproteomic and proteomic analysis was conducted to connect molecular perturbations to the phenotypic changes. Results: We identified an association between metastasis-related properties of TRAP-overexpressing MDA-MB-231 breast cancer cells and a TRAP-dependent regulation of Transforming growth factor (TGF?) pathway proteins and Cluster of differentiation 44 (CD44). Overexpression of TRAP increased anchorage-independent and anchorage-dependent cell growth and proliferation, induced a more elongated cellular morphology and promoted cell migration and invasion. Migration was increased in the presence of the extracellular matrix (ECM) proteins osteopontin and fibronectin and the basement membrane proteins collagen IV and laminin I. TRAP-induced properties were reverted upon shRNA-mediated knockdown of TRAP or treatment with the small molecule TRAP inhibitor 5-PNA. Global phosphoproteomics and proteomics analyses identified possible substrates of TRAP phosphatase activity or signaling intermediates and outlined a TRAP-dependent regulation of proteins involved in cell adhesion and ECM organization. Upregulation of TGF? isoform 2 (TGF?2), TGF? receptor type 1 (T?R1) and Mothers against decapentaplegic homolog 2 (SMAD2), as well as increased intracellular phosphorylation of CD44 were identified upon TRAP perturbation. Functional antibody-mediated blocking and chemical inhibition demonstrated that TRAP-dependent migration and proliferation is regulated via TGF?2/T?R, whereas proliferation beyond basal levels is regulated through CD44. Conclusion: Altogether, TRAP promotes metastasis-related cell properties in MDA-MB-231 breast cancer cells via TGF?2/T?R and CD44, thereby identifying a potential signaling mechanism associated to TRAP action in breast cancer cells. Electronic supplementary material: The online version of this article doi:(10.1186/s12885-017-3616-7) contains supplementary material, which is available to authorized users. äTartrate-resistant acid phosphatase (TRAP/ACP5) promotes metastasis-re(epmc).pdf DeepDyve Pubget Overpricing