TNFSF9 promotes metastasis of pancreatic cancer by regulating M2 polarization of macrophages through Src/FAK/p-Akt/IL-1β signaling

被引：21
作者：
Wu, Jiao [1 ]
Wang, Yunpeng [2 ]
Yang, Yichun [1 ]
Liu, Fuqiang [1 ]
Jiang, Zhongxiang [1 ]
Jiang, Zheng [1 ]
机构：
[1] Chongqing Med Univ, Affiliated Hosp 1, Dept Gastroenterol, Chongqing 400016, Peoples R China
[2] Zigong First Peoples Hosp, Dept Cardiovasc, Sichuan 643000, Peoples R China
来源：
INTERNATIONAL IMMUNOPHARMACOLOGY | 2022年 / 102卷
关键词：
TNFSF9; Pancreatic cancer; Macrophages; Polarization; Meatastasis; BREAST-CANCER; BONE METASTASIS; CD137; LIGAND; CELLS; SRC;
D O I：
10.1016/j.intimp.2021.108429
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
The effect of tumor necrosis factor superfamily member 9 (TNFSF9) on the metastasis of pancreatic cancer (PC) and the underlying mechanism remain unclear. We studied the expression of TNFSF9 in pancreatic cancer and its relationship with immune cells. We further explored the effect of TNFSF9 on pancreatic cancer metastasis by inducing macrophage polarization, and evaluated the expression of Src/FAK/p-Akt/IL-1 beta signals in macrophages after knocking down TNFSF9. The data shows that TNFSF9 expression is elevated in pancreatic cancer and is related to the poor prognosis of patients with pancreatic cancer. In addition, TNFSF9 may induce the M2 polarization of macrophages through Src/FAK/p-Akt/IL-1 beta signals, thereby promoting the migration of pancreatic cancer cells. In conclusion, our data reveals that TNFSF9 may become a predictive biomarker of pancreatic cancer and provides a new intervention target for the immunotherapy of pancreatic cancer.
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页数：11
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