{"database":"biostudies-literature","file_versions":[],"scores":{"citationCount":0,"reanalysisCount":0,"viewCount":49,"searchCount":0},"additional":{"omics_type":["Unknown"],"volume":["12(6)"],"submitter":["Zhao P"],"pubmed_abstract":["Response gene to complement 32 (RGC-32) is a cell cycle regulator involved in the proliferation, differentiation and migration of cells and has also been implicated in angiogenesis. Here we show that RGC-32 expression in macrophages is induced by IL-4 and reduced by LPS, indicating a link between RGC-32 expression and M2 polarization. We demonstrated that the increased expression of RGC-32 is characteristic of alternatively activated macrophages, in which this protein suppresses the production of pro-inflammatory cytokine IL-6 and promotes the production of the anti-inflammatory mediator TGF-β. Consistent with in vitro data, tumor-associated macrophages (TAMs) express high levels of RGC-32, and this expression is induced by tumor-derived ascitic fluid in an M-CSF- and/or IL-4-dependent manner. Collectively, these results establish RGC-32 as a marker for M2 macrophage polarization and indicate that this protein is a potential target for cancer immunotherapy, targeting tumor-associated macrophages."],"journal":["Cellular & molecular immunology"],"pagination":["692-9"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4716617"],"repository":["biostudies-literature"],"pubmed_title":["Response gene to complement 32 (RGC-32) expression on M2-polarized and tumor-associated macrophages is M-CSF-dependent and enhanced by tumor-derived IL-4."],"pmcid":["PMC4716617"],"pubmed_authors":["Ji C","Li X","Wang Q","Song B","Zhao P","Li P","Qu X","Shao Q","Sun J","Gao D"],"view_count":["49"],"additional_accession":[]},"is_claimable":false,"name":"Response gene to complement 32 (RGC-32) expression on M2-polarized and tumor-associated macrophages is M-CSF-dependent and enhanced by tumor-derived IL-4.","description":"Response gene to complement 32 (RGC-32) is a cell cycle regulator involved in the proliferation, differentiation and migration of cells and has also been implicated in angiogenesis. Here we show that RGC-32 expression in macrophages is induced by IL-4 and reduced by LPS, indicating a link between RGC-32 expression and M2 polarization. We demonstrated that the increased expression of RGC-32 is characteristic of alternatively activated macrophages, in which this protein suppresses the production of pro-inflammatory cytokine IL-6 and promotes the production of the anti-inflammatory mediator TGF-β. Consistent with in vitro data, tumor-associated macrophages (TAMs) express high levels of RGC-32, and this expression is induced by tumor-derived ascitic fluid in an M-CSF- and/or IL-4-dependent manner. Collectively, these results establish RGC-32 as a marker for M2 macrophage polarization and indicate that this protein is a potential target for cancer immunotherapy, targeting tumor-associated macrophages.","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 Nov","modification":"2024-10-17T16:11:06.828Z","creation":"2019-03-27T02:07:03Z"},"accession":"S-EPMC4716617","cross_references":{"pubmed":["25418473"],"doi":["10.1038/cmi.2014.108"]}}