CCR5 blockade reduces tumor growth by inducing apoptosis and impairing immunosuppression of tumor microenvironment
10.3969/j.issn.1006-5725.2024.09.005
- VernacularTitle:拮抗CC趋化因子受体5信号诱导肿瘤细胞凋亡并调节肿瘤微环境抑制肿瘤生长
- Author:
Wei HE
1
;
Liping LIU
;
Jingwei ZHUO
;
Xiaodong ZHANG
;
Tong YANG
;
Jubin FENG
Author Information
1. 广州医科大学附属第二医院(广州 510260)
- Keywords:
CC-chemokine receptor 5;
tumor microenvironment;
apoptosis;
regulatory T cell
- From:
The Journal of Practical Medicine
2024;40(9):1204-1210
- CountryChina
- Language:Chinese
-
Abstract:
Objective The present study aimed to explore the effects of CC-chemokine receptor 5 antagonism on tumor growth and immune microenvironment.Methods Cell Counting Kit-8 was used to detect in vitro anti-proliferation activity of maraviroc,a selective CC-chemokine receptor 5 inhibitor,on Lewis cells,a mouse lung adenocarcinoma cell strain.Flow cytometry and real-time quantitative PCR were respectively used to detect cell apop-tosis and Caspase 8 gene expression.In a congenic mouse lung cancer model,the mice were intraperitoneally admin-istered with maraviroc or vehicle.Tumor sizes were measured and tumor infiltrating CD4+,CD8+ and Foxp3+ cells were determined by immunofluorescent staining.Results Our results showed that maraviroc could inhibit the growth of Lewis cancer cells not only in vitro but also in vivo.This in-vitro inhibition was presumably attributable to apoptosis induction by the enhancement of Caspase 8 gene expression after maraviroc blockade.Additionally,more CD4+ and CD8+ cells but less Foxp3+ cells were detected in tumor mass from the mice administered with maraviroc.Conclusions Taken together,it can be speculated that CCR5 blockade may inhibit the growth of Lewis cells by inducing cell apoptosis and impairing the immunosuppressive tumor microenvironment.It is worthy of further investi-gation as a candidate for cancer therapy.
