S-allylmercaptocysteine promotes anti-tumor immunity by suppressing PD-L1 expression

被引:2
|
作者
Zhao, Zhongxi [4 ]
Wei, Guangwei [5 ]
Zhao, Jianxiong [1 ]
Sun, Yueyue [2 ]
Gao, Peng [3 ]
机构
[1] Shandong Univ, Cheeloo Coll Med, Sch Basic Med Sci, Dept Anat,Key Lab Expt Teratol Minist Educ, Jinan, Peoples R China
[2] Shandong Univ, Shandong Key Univ Lab Pharmaceut & Drug Delivery S, Cheeloo Coll Med, Sch Pharmaceut Sci, Jinan, Peoples R China
[3] Shandong Univ, Cheeloo Coll Med, Sch Basic Med Sci, Key Lab Expt Teratol Minist Educ,Dept Pathol, Jinan, Peoples R China
[4] Shandong Univ, Cheeloo Coll Med, Sch Pharmaceut Sci, Jinan, Peoples R China
[5] Shandong Univ, Cheeloo Coll Med, Sch Basic Med Sci, Dept Cell Biol, Jinan, Peoples R China
基金
中国国家自然科学基金;
关键词
Immune check -point; PD-L1; Small molecules; S-allylmercaptocysteine; Immunotherapy; CANCER CELLS; APOPTOSIS; INDUCTION; VIVO;
D O I
10.1016/j.biopha.2023.114446
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
SAMC (S-allylmercaptocysteine) possesses significant anti-tumor effects and is proven to inhibit inflammation in chronic obstructive pulmonary disease. The potential to regulate the immune system of SAMC inspired us to detect whether SAMC can promote anti-tumor immunity. Here we found that SAMC inhibits tumor development and progression by boosting CD8+ T cell and NK cell infiltration and decreasing the frequency of immune suppressing Treg cells in tumor tissue and enhancing the systemic immune function. Mechanistically, we found that SAMC suppresses PD-L1 expression at transcriptional level to increase the activation of anti-tumor cytotoxic T cells. Finally, we proved that SAMC inhibits PD-L1 transcription by suppressing the phosphorylation activation of STAT3. In conclusion, our findings reveal that SAMC is a potent immunity regulator and a potential agent for immune checkpoint inhibition in tumor therapy.
引用
收藏
页数:11
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