scholarly journals Specific ligands of the peripheral benzodiazepine receptor induce apoptosis and cell cycle arrest in human esophageal cancer cells

2002 ◽  
Vol 102 (4) ◽  
pp. 318-327 ◽  
Author(s):  
Andreas P. Sutter ◽  
Kerstin Maaser ◽  
Michael Höpfner ◽  
Bettina Barthel ◽  
Patricia Grabowski ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Esophageal Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Benzodiazepine Receptor ◽  
Peripheral Benzodiazepine Receptor ◽  
Cycle Arrest ◽  
Human Esophageal Cancer ◽  
Esophageal Cancer Cells

Specific ligands of the peripheral benzodiazepine receptor induce apoptosis and cell cycle arrest in human esophageal cancer cells

2001 ◽  
Vol 120 (5) ◽  
pp. A444
Author(s):  
Andreas Sutter ◽  
Kerstin Maaser ◽  
Bettina Barthel ◽  
Bernd Von Lampe ◽  
Ernst-Otto Riecken ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Esophageal Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Benzodiazepine Receptor ◽  
Peripheral Benzodiazepine Receptor ◽  
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.

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