» Articles » PMID: 25418473

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

Overview
Date 2014 Nov 25
PMID 25418473
Citations 36
Authors
Affiliations
Soon will be listed here.
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.

Citing Articles

Response Gene to Complement 32 is associated with poor patient survival and an inflamed tumor-immune microenvironment in clear cell renal cell carcinoma.

Li L, Bu X, Wang S, Liu Y, Chen C, Zhang W Transl Oncol. 2024; 52:102248.

PMID: 39709718 PMC: 11832949. DOI: 10.1016/j.tranon.2024.102248.


Metformin Inhibits the Progression of Pancreatic Cancer Through Regulating miR-378a-3p/VEGFA/RGC-32 Axis.

He J, Luo Y, Ding Y, Zhu L Cancer Med. 2024; 13(23):e70446.

PMID: 39606802 PMC: 11602749. DOI: 10.1002/cam4.70446.


PTGR1-mediated immune evasion mechanisms in late-stage triple-negative breast cancer: mechanisms of M2 macrophage infiltration and CD8 T cell suppression.

Huang F, Wang F, Hu Q, Li Y, Jiang D Apoptosis. 2024; 29(11-12):2002-2024.

PMID: 39068625 DOI: 10.1007/s10495-024-01991-0.


A novel single-cell model reveals ferroptosis-associated biomarkers for individualized therapy and prognostic prediction in hepatocellular carcinoma.

Zhou Q, Tao C, Ge Y, Yuan J, Pan F, Lin X BMC Biol. 2024; 22(1):133.

PMID: 38853238 PMC: 11163722. DOI: 10.1186/s12915-024-01931-z.


Tumor-associated macrophages, dendritic cells, and neutrophils: biological roles, crosstalk, and therapeutic relevance.

Shen M, Du Y, Ye Y Med Rev (2021). 2023; 1(2):222-243.

PMID: 37724296 PMC: 10388790. DOI: 10.1515/mr-2021-0014.


References
1.
Shao Q, Ning H, Lv J, Liu Y, Zhao X, Ren G . Regulation of Th1/Th2 polarization by tissue inhibitor of metalloproteinase-3 via modulating dendritic cells. Blood. 2012; 119(20):4636-44. DOI: 10.1182/blood-2011-08-376418. View

2.
Badea T, Niculescu F, Soane L, Fosbrink M, Sorana H, Rus V . RGC-32 increases p34CDC2 kinase activity and entry of aortic smooth muscle cells into S-phase. J Biol Chem. 2001; 277(1):502-8. DOI: 10.1074/jbc.M109354200. View

3.
Menen R, Hassanein M, Momiyama M, Suetsugu A, Moossa A, Hoffman R . Tumor-educated macrophages promote tumor growth and peritoneal metastasis in an orthotopic nude mouse model of human pancreatic cancer. In Vivo. 2012; 26(4):565-9. View

4.
Biswas S, Allavena P, Mantovani A . Tumor-associated macrophages: functional diversity, clinical significance, and open questions. Semin Immunopathol. 2013; 35(5):585-600. DOI: 10.1007/s00281-013-0367-7. View

5.
Mantovani A, Sica A, Sozzani S, Allavena P, Vecchi A, Locati M . The chemokine system in diverse forms of macrophage activation and polarization. Trends Immunol. 2004; 25(12):677-86. DOI: 10.1016/j.it.2004.09.015. View