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10.18632/oncotarget.6414 http://scihub22266oqcxt.onion/10.18632/oncotarget.6414 C4811478!4811478 !26625314     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26625314 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Oncotarget 2016 ; 7 (2 ): 1529-43 Nephropedia Template TP {{tp|p=26625314 |t=2016. Critical role of PPAR? in myeloid-derived suppressor cell-stimulated cancer cell proliferation and metastasis |pdf=|usr=}}{{26625314 }} gab.com Text Critical role of PPAR in myeloid-derived suppressor cell-stimulated cancer cell proliferation and metastasis JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26625314 #FOAvip Lysosomal acid lipase (LAL) is a key enzyme controlling neutral lipid metabolic signaling in myeloid-derived suppressor cells (MDSCs). MDSCs from LAL-deficient (lal-/-) mice directly stimulate cancer cell proliferation. PPAR? ligand treatment inhibited lal-/- MDSCs stimulation of tumor cell growth and metastasis in vivo, and tumor cell proliferation and migration in vitro. In addition, PPAR? ligand treatment impaired lal-/- MDSCs transendothelial migration, and differentiation from lineage-negative cells. The corrective effects of PPAR? ligand on lal-/- MDSCs functions were mediated by regulating the mammalian target of rapamycin (mTOR) pathway, and subsequently blocking MDSCs ROS overproduction. Furthermore, in the myeloid-specific dominant-negative PPAR? (dnPPAR?) overexpression bitransgenic mouse model, tumor growth and metastasis were enhanced, and MDSCs from these mice stimulated tumor cell proliferation and migration. MDSCs with dnPPAR? overexpression showed increased transendothelial migration, overactivation of the mTOR pathway, and ROS overproduction. These results indicate that PPAR? plays a critical role in neutral lipid metabolic signaling controlled by LAL, which provides a mechanistic basis for clinically targeting MDSCs to reduce the risk of cancer proliferation, growth and metastasis. Twit Text FOAVip Critical role of PPAR in myeloid-derived suppressor cell-stimulated cancer cell proliferation and metastasis ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26625314 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26625314 #FOAvip English Wikipedia <ref>{{Cite pmid|26625314 }}</ref> Critical role of PPAR? in myeloid-derived suppressor cell-stimulated cancer cell proliferation and metastasis #MMPMID26625314 Zhao T ; Du H ; Blum JS ; Yan C Oncotarget 2016[Jan]; 7 (2 ): 1529-43 PMID26625314 show ga Lysosomal acid lipase (LAL) is a key enzyme controlling neutral lipid metabolic signaling in myeloid-derived suppressor cells (MDSCs). MDSCs from LAL-deficient (lal-/-) mice directly stimulate cancer cell proliferation. PPAR? ligand treatment inhibited lal-/- MDSCs stimulation of tumor cell growth and metastasis in vivo, and tumor cell proliferation and migration in vitro. In addition, PPAR? ligand treatment impaired lal-/- MDSCs transendothelial migration, and differentiation from lineage-negative cells. The corrective effects of PPAR? ligand on lal-/- MDSCs functions were mediated by regulating the mammalian target of rapamycin (mTOR) pathway, and subsequently blocking MDSCs ROS overproduction. Furthermore, in the myeloid-specific dominant-negative PPAR? (dnPPAR?) overexpression bitransgenic mouse model, tumor growth and metastasis were enhanced, and MDSCs from these mice stimulated tumor cell proliferation and migration. MDSCs with dnPPAR? overexpression showed increased transendothelial migration, overactivation of the mTOR pathway, and ROS overproduction. These results indicate that PPAR? plays a critical role in neutral lipid metabolic signaling controlled by LAL, which provides a mechanistic basis for clinically targeting MDSCs to reduce the risk of cancer proliferation, growth and metastasis. |*Cell Communication/drug effects [MESH] |*Cell Movement/drug effects [MESH] |*Cell Proliferation/drug effects [MESH] |Animals [MESH] |Antigens, Ly/metabolism [MESH] |Carcinoma, Lewis Lung/genetics/*metabolism/secondary [MESH] |Cell Differentiation [MESH] |Cell Line, Tumor [MESH] |Coculture Techniques [MESH] |Genetic Predisposition to Disease [MESH] |Linoleic Acids, Conjugated/pharmacology [MESH] |Melanoma, Experimental/genetics/*metabolism/secondary [MESH] |Membrane Potential, Mitochondrial [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Myeloid Cells/drug effects/*metabolism [MESH] |PPAR gamma/agonists/genetics/*metabolism [MESH] |Phenotype [MESH] |Reactive Oxygen Species/metabolism [MESH] |Signal Transduction [MESH] |Skin Neoplasms/genetics/*metabolism/pathology [MESH] |Sterol Esterase/deficiency/genetics [MESH] |TOR Serine-Threonine Kinases/metabolism [MESH] |Time Factors [MESH] |Transendothelial and Transepithelial Migration [MESH] |Transfection [MESH]Critical role of PPAR? in myeloid-derived suppressor cell-stimulated c(epmc).pdf DeepDyve Pubget Overpricing