溶血磷脂酸
自交轴蛋白
癌症研究
细胞生长
蛋白激酶B
PI3K/AKT/mTOR通路
细胞迁移
化学
细胞
信号转导
生物
受体
生物化学
作者
Si Liu,Haiyan Jiang,Li Min,Tingting Ning,Junxuan Xu,Tiange Wang,Xingyu Wang,Qian Zhang,Ruizhen Cao,Shutian Zhang,Shoumin Zhu
出处
期刊:Carcinogenesis
[Oxford University Press]
日期:2020-12-28
卷期号:42 (4): 611-620
被引量:7
标识
DOI:10.1093/carcin/bgaa143
摘要
Abstract Lysophosphatidic acid (LPA) and its G-protein-coupled receptors (Lpar1–Lpar6) mediate a plethora of activities associated with cancer growth and progression. However, there is no systematic study about whether and how LPA promotes esophageal squamous cell carcinoma (ESCC). Here, we show that autotaxin (ATX), a primary LPA-producing enzyme, is highly expressed in ESCC, and overexpressed ATX is associated with the poor outcome of ESCC patients. Meanwhile, the expression of Lpar1 was much higher in ESCC cells compared with Het-1a (human esophagus normal epithelial cells). Functional experiments showed that LPA remarkably increased the proliferation and migration of ESCC cells. Furthermore, Lpar1 knockdown abolished the effect of LPA on ESCC cell proliferation and migration. Mechanistic studies revealed that LPA promoted ESCC cell lines proliferation and migration through PI3K/Akt pathway. Treatment of KYSE30 cell xenografts with Lpar1 inhibitor BMS-986020 significantly repressed tumor growth. Our results shed light on the important role of LPA in ESCC, and Lpar1 might be a potential treatment target for ESCC.
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