趋化因子
癌症研究
结直肠癌
血管生成
肿瘤进展
生物
转移
癌症
癌变
下调和上调
剖腹手术
新生血管
髓源性抑制细胞
免疫学
腹膜腔
医学
病理
免疫系统
抑制器
外科
解剖
基因
生物化学
遗传学
作者
Pingbo Xu,Hong He,Yuechao Gu,Yun Wang,Zhirong Sun,Li Yang,Changhong Miao
标识
DOI:10.1016/j.yexcr.2018.07.035
摘要
Surgical stress has been shown to facilitate the tumor growth and metastasis of colon cancer. To unravel the mechanisms underlying surgery induced-colon cancer progression, a syngeneic transplantation tumor model was established with murine colon cancer CT26 cells and the effect of laparotomy on tumor progression was investigated. Especially the expression of several CXC chemokines was assayed, and its roles in regulating myeloid-derived suppressor cells (MDSCs) recruitment were analyzed. We found that laparotomy promoted in vivo tumor growth and angiogenesis. CXCL4 expression was significantly downregulated by laparotomy in the tumor tissue and the peritoneal cavity. Functionally, CXCL4 overexpression significantly reduces tumor volume compared to control. Through analysis of CD11b+/Gr1+ MDSCs cell, we found an upregulated proportion of MDSCs in the tumor tissues and peritoneal cavity following laparotomy, and this enhancement was blocked after CXCL4 overexpression. Further, a negative correlation was found between CXCL4 expression and MDSC amounts in clinical samples. Higher CXCL4 expression and lower MDSCs proportion is positively related to overall survival.Surgical trauma contributes to colon cancer progression by downregulating CXCL4 and hence promoting MDSC recruitment, which leads to an immunosuppressive environment.
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