TP53TG1/STAT axis is involved in the development of colon cancer through affecting PD-L1 expression and immune escape mechanism of tumor cells

被引:0
|
作者
Ji, Wenmin [1 ,3 ]
Wang, Wenyan [2 ]
Wei, Yanfang [1 ]
机构
[1] Shanxi Med Univ, Hosp 1, Taiyuan 030001, Shanxi, Peoples R China
[2] Shanxi Inst Food & Drug Control, Taiyuan 030001, Shanxi, Peoples R China
[3] Shanxi Med Univ, Hosp 1, 85 Jiefang South Rd, Taiyuan 030000, Shanxi, Peoples R China
来源
AMERICAN JOURNAL OF CANCER RESEARCH | 2023年 / 13卷 / 11期
关键词
PD-1/PD-L1; TP53TG1; immune escape; STAT pathway; colon cancer; REGULATORY T-CELLS; LONG NONCODING RNA; CD8(+) T; IMMUNOTHERAPY; COMBINATION; THERAPY; TARGET; RESISTANCE; PROGNOSIS; CD4(+);
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
This research is dedicated to investigating the mechanism of programmed cell death ligand 1 (PD-L1) and tumor protein 53 target gene 1 (TP53TG1) in immune regulation of colon cancer (CC). Expressions of TP53TG1, PDL1 and signal transducers and activators of transcription (STATs) in CC and their correlation were detected through bioinformatics analysis. Effects of PD-L1 and TP53TG1 on the CC were assessed by in vivo and in vitro experiments. Herein, PD-L1 level was negatively correlated with TP53TG1 expression, but was positively correlated with the levels of STATs. Both overexpressed TP53TG1 and PD-L1 antibody reversed the effects of CT26 cells on inhibiting cell proliferation, cytokine secretion and PD-L1 level, and enhancing the cytotoxicity of NK cells and CD8+ T cells. TP53TG1 reduced PD-L1 level by inactivating STATs pathway. Downregulation of PD-L1 increased cytokine secretion and T lymphocyte killing ability, promoted tumor cell apoptosis, and inhibited the tumor growth. Altogether, TP53TG1/STAT axis regulates the immunomodulatory mechanism of CC by reducing PD-L1 expression.
引用
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页码:5218 / +
页数:19
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