Chloride ions control the G1/S cell-cycle checkpoint by regulating the expression of p21 through a p53-independent pathway in human gastric cancer cells

2008 ◽  
Vol 366 (2) ◽  
pp. 506-512 ◽  
Author(s):  
Hiroaki Miyazaki ◽  
Atsushi Shiozaki ◽  
Naomi Niisato ◽  
Rumi Ohsawa ◽  
Hirosumi Itoi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Chloride Ions ◽  
Cell Cycle Checkpoint ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Cycle Checkpoint

scholarly journals The Effect of Docetaxel (Taxotere®) on Human Gastric Cancer Cells Exhibiting Low-Dose Radiation Hypersensitivity

2008 ◽  
Vol 2 ◽  
pp. CMO.S463
Author(s):  
Elizabeth K. Balcer-Kubiczek ◽  
Mona Attarpour ◽  
Jian Z. Wang ◽  
William F. Regine
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Time Course ◽  
Low Dose ◽  
Immunoblot Analysis ◽  
Human Gastric Cancer ◽  
Low Dose Radiation ◽  
Gastric Cancer Cells ◽  
Dose Radiation

Low-dose radiation hypersensitivity (HRS) describes a phenomenon of excessive sensitivity to X ray doses <0.5 Gy. Docetaxel is a taxane shown to arrest cells in the G2/M phase of the cell cycle. Some previous studies suggested that HRS might result from the abrogation of the early G2 checkpoint arrest. First we tested whether HRS occurs in gastric cancer—derived cells, and whether pre-treatment of cells with low docetaxel concentrations can enhance the magnitude of HRS in gastric cancer cells. The results demonstrated HRS at ~0.3 Gy and the synergy between 0.3 Gy and docetaxel (3 nM for 24 h), and the additivity of other drug/dose combinations. The synergistic effect was associated with a significant docetaxel-induced G2 accumulation. Next, we evaluated in time-course experiments ATM kinase activity and proteins associated with the induction and maintenance of the early G2 checkpoint. The results of multi-immunoblot analysis demonstrate that HRS does not correlate with the ATM-dependent early G2 checkpoint arrest. We speculate that G2 checkpoint adaptation, a phenomenon associated with a prolonged cell cycle arrest, might be involved in HRS. Our results also suggest a new approach for the improvement the effectiveness of docetaxel-based radiotherapy using low doses per fraction.

scholarly journals Ailanthone induces G2/M cell cycle arrest and apoptosis of SGC-7901 human gastric cancer cells

2017 ◽  
Vol 16 (5) ◽  
pp. 6821-6827 ◽  
Author(s):  
Yuxin Chen ◽  
Ling Zhu ◽  
Xi Yang ◽  
Cheng Wei ◽  
Chuanrong Chen ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Human Gastric Cancer ◽  
M Cell ◽  
Gastric Cancer Cells ◽  
Cycle Arrest

The Effect of Quercetin and Other Flavonoids on Cell Cycle Progression and Growth of Human Gastric Cancer Cells

Planta Medica ◽  
1990 ◽  
Vol 56 (06) ◽  
pp. 677-678 ◽  
Author(s):  
Y. Matsukawa ◽  
M. Yoshida ◽  
T Sakai ◽  
N. Marui ◽  
K. Matsumoto ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Cell Cycle Progression ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Cycle Progression

scholarly journals Gramicidin inhibits human gastric cancer cell proliferation, cell cycle and induced apoptosis

2019 ◽  
Vol 52 (1) ◽  
Author(s):  
Tingting Chen ◽  
Yong Wang ◽  
Yang Yang ◽  
Kaikai Yu ◽  
Xiangliao Cao ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
High Morbidity ◽  
Peptide Antibiotic ◽  
Human Gastric Cancer ◽  
M Cell ◽  
Gastric Cancer Cells ◽  
Gastric Mucosal Cells ◽  
Mucosal Cells

Abstract Background Gastric cancer is a common malignant tumor with high morbidity and mortality worldwide, which seriously affects human health. Gramicidin is a short peptide antibiotic which could be used for treating infection induced by bacteria or fungi. However, the anti-cancer effect of gramicidin on gastric cancer cells and its underlying mechanism remains largely unknown. Results Gastric cancer cells SGC-7901, BGC-823 and normal gastric mucosal cells GES-1 were treated with different concentrations of gramicidin respectively. The results of CCK-8 experiment revealed cellular toxicity of gramicidin to cancer cells while cell colony formation assay showed that gramicidin significantly inhibited the proliferation of gastric cancer cells, but had little effect on normal gastric mucosal cells. In addition, the wound healing assay showed that gramicidin inhibited the migration of SGC-7901 cell. Meanwhile, apoptosis and cell cycle analysis revealed that gramicidin induced cell apoptosis with G2/M cell cycle inhibition. Furthermore, western blot analysis demonstrated that gramicidin down-regulated the expression of cyclinD1 and Bcl-2 as well as the FoxO1 phosphorylation. Conclusions The current study illustrated the anti-tumor activity of gramicidin on gastric cancer cells, providing a possibility for gramicidin to be applied in clinical practice for the treatment of gastric cancer.

Antiproliferative mechanism of a cannabinoid agonist by cell cycle arrest in human gastric cancer cells

2011 ◽  
Vol 112 (4) ◽  
pp. 1192-1205 ◽  
Author(s):  
Jae Myung Park ◽  
Xiang-Shu Xian ◽  
Myung-Gyu Choi ◽  
Hyeyeon Park ◽  
Yu Kyung Cho ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Cycle Arrest ◽  
Cannabinoid Agonist
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