scholarly journals 2-Acetylamino-3-[4-(2-acetylamino-2-carboxyethylsulfanylcarbonylamino) phenyl carbamoylsulfanyl] propionic acid, a glutathione reductase inhibitor, induces G2/M cell cycle arrest through generation of thiol oxidative stress in human esophageal cancer cells

Oncotarget ◽  
2017 ◽  
Vol 8 (37) ◽  
pp. 61846-61860 ◽  
Author(s):  
Xia Li ◽  
Zhiming Jiang ◽  
Jianguo Feng ◽  
Xiaoying Zhang ◽  
Junzhou Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Esophageal Cancer ◽  
Glutathione Reductase ◽  
Cancer Cells ◽  
Reductase Inhibitor ◽  
M Cell ◽  
Cycle Arrest ◽  
Human Esophageal Cancer ◽  
Esophageal Cancer Cells

scholarly journals Gypenoside L Inhibits Proliferation of Liver and Esophageal Cancer Cells by Inducing Senescence

Molecules ◽  
2019 ◽  
Vol 24 (6) ◽  
pp. 1054 ◽  
Author(s):  
Jingxin Ma ◽  
Xiaopeng Hu ◽  
Chenghui Liao ◽  
Haitao Xiao ◽  
Qinchang Zhu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Esophageal Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Inhibitory Effect ◽  
Cancer Cell Growth ◽  
Therapeutic Drugs ◽  
Cycle Arrest ◽  
Chemical Inhibitors ◽  
Esophageal Cancer Cells

Senescence is an irreversible state of cell cycle arrest that can be triggered by multiple stimuli, such as oxygen reactive species and DNA damage. Growing evidence has proven that senescence is a tumor-suppressive approach in cancer treatment. Therefore, developing novel agents that modulate senescence may be an alternative strategy against cancer. In our study, we investigated the inhibitory effect of gypenoside L (Gyp-L), a saponin isolated from Gynostemma pentaphyllum, on cancer cell growth. We found that Gyp-L increased the SA-β-galactosidase activity, promoted the production of senescence-associated secretory cytokines, and inhibited cell proliferation of human liver and esophageal cancer cells. Moreover, Gyp-L caused cell cycle arrest at S phase, and activated senescence-related cell cycle inhibitor proteins (p21 and p27) and their upstream regulators. In addition, Gyp-L activated p38 and ERK MAPK pathways and NF-κB pathway to induce senescence. Consistently, adding chemical inhibitors efficiently counteracted the Gyp-L-mediated senescence, growth inhibition, and cell cycle arrest in cancer cells. Furthermore, treatment with Gyp-L, enhanced the cytotoxicity of clinic therapeutic drugs, including 5-fluorouracil and cisplatin, on cancer cells. Overall, these results indicate that Gyp-L inhibits proliferation of cancer cells by inducing senescence and renders cancer cells more sensitive to chemotherapy.

scholarly journals Autophagy-dependent cell cycle arrest in esophageal cancer cells exposed to dihydroartemisinin

2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Qiang Ma ◽  
Hebin Liao ◽  
Lei Xu ◽  
Qingrong Li ◽  
Jiang Zou ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Esophageal Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Cycle Arrest ◽  
Dependent Cell ◽  
Esophageal Cancer Cells
Sign in / Sign up

Export Citation Format

Share Document