Effect mechanism of Jaceosidin on immune escape of colorectal cancer cells by regulating cGAS-STING signaling pathway
10.3969/j.issn.1000-484X.2025.03.021
- VernacularTitle:棕矢车菊素通过调节cGAS-STING信号通路影响结直肠癌细胞免疫逃逸的机制研究
- Author:
Yongjie DONG
1
;
Jing DONG
;
Feng YUE
;
Hui JIA
;
Guangchao QIAO
Author Information
1. 邯郸市中心医院普外二科,邯郸 056001
- Publication Type:Journal Article
- Keywords:
Jaceosidin;
Colorectal cancer;
Cyclic guanosine monophosphate-adenylate synthase-stimulator of interferon gene signaling pathway;
Proliferation;
Apoptosis;
Immune escape
- From:
Chinese Journal of Immunology
2025;41(3):634-639
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effect of Jaceosidin on immune escape of colorectal cancer(CRC)cells by regulating cyclic guanosine monophosphate-adenylate synthase(cGAS)-stimulator of interferon gene(STING)signal pathway.Methods:Human CRC cells HCT116 were cultured in vitro and grouped into control group,Jaceosidin-L group(25 μmol/L),Jaceosidin-M group(50 μmol/L),Jaceosidin-H group(100 μmol/L),activator group[100 μmol/L Jaceosidin+10 μmol/L cGAS activator manganese chloride(MnCl2·4H2O)],and inhibitor group(100 μmol/L Jaceosidin+1 μmol/L cGAS inhibitor RU.521);CCK-8 method was applied to de-tect the proliferation of HCT116 cells;flow cytometry was applied to detect apoptosis of HCT116 cells;HCT116 cells were co-cultured with NK cell to detect NK cell killing activity;ELISA was applied to detect the levels of IFN-γ and Granzyme B in the supernatant of co cultured cells;Western blot and qRT-PCR were applied to detect the expression of cGAS-STING signaling pathway and apoptosis related factors.Results:Compared with the control group,the A450 value and Bcl-2 expression of HCT116 cells in the Jaceosidin-L,Ja-ceosidin-M,and Jaceosidin-H groups were obviously reduced,the apoptosis rate,and the expression of cGAS,STING and Bax were obviously increased,and were dose-dependent(P<0.05);compared with the control co culture group,the levels of IFN-γ and Gran-zyme B,and NK cell killing activity in the supernatant of the Jaceosidin-L,Jaceosidin-M,and Jaceosidin-H co culture groups were significantly increased,in a dose-dependent manner(P<0.05);cGAS activator MnCl2·4H2O enhanced the inhibitory effects of high-dose Jaceosidin on HCT116 cell proliferation,immune escape,and the promoting effect on cell apoptosis,cGAS inhibitor RU.521 weakened the inhibitory effects of high-dose Jaceosidin on HCT116 cell proliferation,immune escape,and the promoting effect on cell apoptosis.Conclusion:Jaceosidin inhibits HCT116 cell proliferation,immune escape,and promotes cell apoptosis by activating cGAS-STING signaling pathway.
