ARHGEF39 promotes gastric cancer cell proliferation and migration via Akt signaling pathway

2017 ◽  
Vol 440 (1-2) ◽  
pp. 33-42 ◽  
Author(s):  
Haixiao Wang ◽  
Miaomiao Li ◽  
Xiaobao Tao ◽  
Yan Qian ◽  
Linfang Chen ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Gastric Cancer Cell ◽  
Akt Signaling ◽  
Cancer Cell Proliferation ◽  
Akt Signaling Pathway ◽  
Cell Proliferation And Migration ◽  
Gastric Cancer Cell Proliferation ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals GJB4 promotes gastric cancer cell proliferation and migration via Wnt/CTNNB1 pathway

2019 ◽  
Vol Volume 12 ◽  
pp. 6745-6755 ◽  
Author(s):  
GuiYuan Liu ◽  
Yi Pang ◽  
YaJun Zhang ◽  
HaiRong Fu ◽  
Wei Xiong ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Cell Proliferation And Migration ◽  
Gastric Cancer Cell Proliferation ◽  
And Migration ◽  
Proliferation And Migration

Baicalein Inhibits Gastric Cancer Cell Proliferation and Migration through a FAK Interaction via AKT/mTOR Signaling

2021 ◽  
pp. 1-17
Author(s):  
Dan Qiao ◽  
Jingchun Jin ◽  
Jian Xing ◽  
Yingying Zhang ◽  
Nailing Jia ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Dependent Manner ◽  
Cancer Cell Proliferation ◽  
Cell Proliferation And Migration ◽  
Gastric Cancer Cell Proliferation ◽  
And Migration ◽  
Proliferation And Migration

Gastric cancer is a common malignancy worldwide and is associated with high morbidity and mortality rates. However, very little is known about the underlying mechanism in human gastric cancer cells. Baicalein (BAI), a widely used Chinese herbal medicine, has shown anticancer effects on many types of human cancer cell lines. Here, we investigated the molecular mechanisms underlying BAI action on gastric cancer cell proliferation and migration. The results showed that BAI can expressively inhibit cell proliferation, colony-forming ability and migration ability in a dose-dependent manner, while in the meantime inducing cell apoptosis. Additionally, we found that BAI can suppress FAK and the phosphorylation of PI3K, AKT and mTOR in a dose-dependent manner. Furthermore, BAI significantly inhibited tumor growth in a xenograft model. Also, BAI can inhibit the proliferation and migration of gastric cancer cells and the expression of the pathway by downregulating the expression of FAK. In short, we demonstrated that BAI inhibited gastric cancer cell proliferation and migration through FAK interaction via downregulation in AKT/mTOR signaling, which signifies that BAI may be a latent therapeutic factor for the treatment of gastric cancer patients and that FAK might be a hopeful therapy target for the disease.

Sign in / Sign up

Export Citation Format

Share Document