The response gene to complement (RGC)-32 acts as a cell cycle regulator and mediator of TGF-β effects. However, recent studies have revealed other functions for RGC-32 in diverse processes such as cellular migration, differentiation, and fibrosis. In addition to its induction by complement activation and the C5b-9 terminal complement complex, RGC-32 expression is also stimulated by growth factors, hormones, and cytokines. RGC-32 is induced by TGF-β through Smad3 and RhoA signaling and plays an important role in cell differentiation. In particular, RGC-32 is essential for the differentiation of Th17 cells. RGC-32 mice display an attenuated experimental autoimmune encephalomyelitis phenotype that is accompanied by decreased central nervous system inflammation and reductions in IL-17- and GM-CSF-producing CD4 T cells. Accumulating evidence has drawn attention to the deregulated expression of RGC-32 in human cancers, atherogenesis, metabolic disorders, and autoimmune disease. Furthermore, RGC-32 is a potential therapeutic target in multiple sclerosis and other Th17-mediated autoimmune diseases. A better understanding of the mechanism(s) by which RGC-32 contributes to the pathogenesis of all these diseases will provide new insights into its therapeutic potential.
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Article Synopsis
- Systemic lupus erythematosus is an autoimmune disease causing damage to kidneys and organs, which was studied in the context of nephrotoxic nephritis (NTN) as a model for lupus nephritis.
- The research focused on response gene to complement-32 (RGC-32), finding that its absence in RGC-32 knockout (KO) NTN mice led to reduced proteinuria, improved kidney function, and less severe kidney damage.
- RGC-32 KO mice also showed decreased recruitment of certain immune cells and less renal fibrosis, suggesting that RGC-32 could be a promising target for new treatments aimed at combatting conditions like lupus nephritis.
RGC-32 facilitates pancreatic cancer via activating Wnt/β-catenin signaling.
Cell Mol Biol (Noisy-le-grand)
December 2023
Department of Gastroenterology, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.
Longitudinal studies have indicated the facilitating effect of RGC-32 during diverse disease progression including pancreatic cancer, yet the systematic and detailed effect of RGC-32 during pancreatic cancer is largely unknowable. For this purpose, we took advantage of the pancreatic cancer cell line (BXPC3) with RGC-32 expression and then modulated its expression by lentivirus-mediated knockdown (shRGC-32) and overexpression (pcDNA-RGC-32). To verify the effect of Wnt/β-catenin signaling in RGC-32-based tumorigenicity, we added the agonist CT99021 to the shRGC-32 BXPC3 cell line and pancreatic cancer mouse model.
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