生物
癌症研究
PI3K/AKT/mTOR通路
血管生成
血管内皮生长因子A
转移
下调和上调
蛋白激酶B
巨噬细胞
癌症
结直肠癌
肿瘤微环境
信号转导
免疫学
细胞生物学
血管内皮生长因子
血管内皮生长因子受体
体外
生物化学
遗传学
肿瘤细胞
基因
作者
Yu Lu,Dandan Fan,Wen Wang,Xian Gao,li hanhan,Shuangshuang Guo,Luyang Zhao,Yaxin Guo,Bowen Li,Yali Zhong,Binglei Zhang,Jingjing Liu,Liping Dai,Qiaozhen Kang,Zhenyu Ji
标识
DOI:10.1016/j.yexcr.2021.112896
摘要
M2 macrophages are crucial components of the tumour microenvironment and have been shown to be closely related to tumour progression. Co-culture with 4.1R−/− M2 macrophages enhances the malignancy of colon cancer (CC), but the mechanism remains unclear. Here, we report that protein 4.1R knockout reduced the phagocytosis of M2 macrophages (M-CSF/IL-4-treated bone marrow cells) and promoted MC38 colon cancer cell proliferation, migration, invasion, tumour formation and epithelial-mesenchymal transition (EMT), which are regulated by M2 macrophages. Further mechanistic dissection revealed that the 4.1R knockout upregulated vascular endothelial growth factor A (VEGFA) secreted by M2 macrophages and promoted colon cancer progression by activating the PI3K/AKT signalling pathway. In summary, our present study identified that 4.1R downregulates VEGFA secretion in M2 macrophages and delays the malignant potential of colon cancer by inhibiting the PI3K/AKT signalling pathway.
科研通智能强力驱动
Strongly Powered by AbleSci AI