Glycitein induces reactive oxygen species‐dependent apoptosis and G0/G1 cell cycle arrest through the MAPK/STAT3/NF‐κB pathway in human gastric cancer cells

Author(s):  
Yan‐Qing Zang ◽  
Yan‐Yu Feng ◽  
Ying‐Hua Luo ◽  
Yu‐Qing Zhai ◽  
Xue‐Ying Ju ◽  
...  
2017 ◽  
Vol 16 (5) ◽  
pp. 6821-6827 ◽  
Author(s):  
Yuxin Chen ◽  
Ling Zhu ◽  
Xi Yang ◽  
Cheng Wei ◽  
Chuanrong Chen ◽  
...  

2011 ◽  
Vol 112 (4) ◽  
pp. 1192-1205 ◽  
Author(s):  
Jae Myung Park ◽  
Xiang-Shu Xian ◽  
Myung-Gyu Choi ◽  
Hyeyeon Park ◽  
Yu Kyung Cho ◽  
...  

2021 ◽  
Vol 16 (1) ◽  
pp. 27-33
Author(s):  
Yi Zhou ◽  
Liguo Wang ◽  
Hui Lin ◽  
Yunxia Wang ◽  
Kezhu Hou

This study was designed to evaluate the anti-cancer effects of bufalin against the human gastric cancer cells and unveil the underlying mechanism. The results showed that bufalin inhibited the proliferation and colony formation of the MGC-803 gastric cancer cells and exhibited an IC50 of 10 μM. These antiproliferative effects were found to be due to the induction of G2/M cell cycle arrest. The G2/M cell cycle arrest was also concomitant with inhibition of cdc2, cdc25 and cyclin B1. Furthermore, bufalin suppressed the epithelial-to-mesenchymal transition, migration, and invasion of the MGC-803 gastric cancer cells. The Western blot analysis revealed that bufalin exerted its effects via deactivation of EK/ERK signaling pathway. Taken together, these results suggest the potential of bufalin as the lead molecule for the development of chemotherapy for gastric cancer.  


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