scholarly journals Stem cells with fused gene expression of cytosine deaminase and interferon-β migrate to human gastric cancer cells and result in synergistic growth inhibition for potential therapeutic use

2011 ◽  
Vol 40 (4) ◽  
pp. 1097-1104 ◽  
Author(s):  
KYOUNG-YOON KIM ◽  
BO-RIM YI ◽  
HYE-RIM LEE ◽  
NAM-HEE KANG ◽  
EUI-BAE JEUNG ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gastric Cancer ◽  
Stem Cells ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Cytosine Deaminase ◽  
Human Gastric Cancer ◽  
Interferon Β ◽  
Gastric Cancer Cells ◽  
Fused Gene

scholarly journals Annonaceous acetogenins mediated up-regulation of Notch2 exerts growth inhibition in human gastric cancer cells in vitro

Oncotarget ◽  
2017 ◽  
Vol 8 (13) ◽  
pp. 21140-21152 ◽  
Author(s):  
Yan Li ◽  
Jianbin Ye ◽  
Zhongbiao Chen ◽  
Junjie Wen ◽  
Fei Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Annonaceous Acetogenins

POT1 deficiency alters telomere length and telomere-associated gene expression in human gastric cancer cells

2010 ◽  
Vol 19 (5) ◽  
pp. 345-351 ◽  
Author(s):  
Xiaoyan Ning ◽  
Shiming Yang ◽  
Rongquan Wang ◽  
Rugang Zhang ◽  
Liping Guo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gastric Cancer ◽  
Cancer Cells ◽  
Telomere Length ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells

Enhanced bax gene expression reduces cell growth and sensitizes human gastric cancer cells to chemotherapeutic agents

2000 ◽  
Vol 118 (4) ◽  
pp. A535
Author(s):  
Koga Komatsu ◽  
Jun-ichi Miyazaki ◽  
Susumu Suzuki ◽  
Michiro Otaka ◽  
Sumio Watanabe ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gastric Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Chemotherapeutic Agents ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Bax Gene

scholarly journals Growth inhibition and induction of apoptosis in SGC-7901 human gastric cancer cells by evodiamine

2014 ◽  
Vol 9 (4) ◽  
pp. 1147-1152 ◽  
Author(s):  
LI YANG ◽  
XIN LIU ◽  
DAN WU ◽  
MAN ZHANG ◽  
GUIPING RAN ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Induction Of Apoptosis

scholarly journals Activated Integrated Stress Response Induced by Salubrinal Promotes Cisplatin Resistance in Human Gastric Cancer Cells via Enhanced xCT Expression and Glutathione Biosynthesis

2018 ◽  
Vol 19 (11) ◽  
pp. 3389 ◽  
Author(s):  
Sheng-Fan Wang ◽  
Chih-Hsuan Wung ◽  
Meng-Shian Chen ◽  
Chian-Feng Chen ◽  
Pen-Hui Yin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gastric Cancer ◽  
Stress Response ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Translation Initiation Factor ◽  
Heme Oxygenase 1 ◽  
Human Gastric Cancer ◽  
Integrated Stress Response ◽  
Gastric Cancer Cells

The integrated stress response (ISR) pathway is essential for adaption of various stresses and is related to mitochondrion-to-nucleus communication. Mitochondrial dysfunction-induced reactive oxygen species (ROS) was demonstrated to activate general control nonderepressible 2 (GCN2)–eukaryotic translation initiation factor 2α (eIF2α)–activating transcription factor-4 (ATF4) pathway-mediated cisplatin resistance of human gastric cancer cells. However, whether or how ISR activation per se could enhance chemoresistance remains unclear. In this study, we used eIF2α phosphatase inhibitor salubrinal to activate the ISR pathway and found that salubrinal reduced susceptibility to cisplatin. Moreover, salubrinal up-regulated ATF4-modulated gene expression, and knockdown of ATF4 attenuated salubrinal-induced drug resistance, suggesting that ATF4-modulated genes contribute to the process. The ATF4-modulated genes, xCT (a cystine/glutamate anti-transporter), tribbles-related protein 3 (TRB3), heme oxygenase 1 (HO-1), and phosphoenolpyruvate carboxykinase 2 (PCK2), were associated with a poorer prognosis for gastric cancer patients. By silencing individual genes, we found that xCT, but not TRB3, HO-1, or PCK2, is responsible for salubrinal-induced cisplatin resistance. In addition, salubrinal increased intracellular glutathione (GSH) and decreased cisplatin-induced lipid peroxidation. Salubrinal-induced cisplatin resistance was attenuated by inhibition of xCT and GSH biosynthesis. In conclusion, our results suggest that ISR activation by salubrinal up-regulates ATF4-modulated gene expression, increases GSH synthesis, and decreases cisplatin-induced oxidative damage, which contribute to cisplatin resistance in gastric cancer cells.

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