scholarly journals Tunicamycin specifically aggravates ER stress and overcomes chemoresistance in multidrug-resistant gastric cancer cells by inhibiting N-glycosylation

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Sheng Chen ◽  
Hao Liu ◽  
Zhe Zhang ◽  
Zhen Ni ◽  
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2016 ◽  
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Yoo Jin Na ◽  
Dae-Hee Lee ◽  
Jung Lim Kim ◽  
Bo Ram Kim ◽  
Seong Hye Park ◽  
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2002 ◽  
Vol 5 (3) ◽  
pp. 154-159 ◽  
Author(s):  
Yongquan Shi ◽  
Ying Han ◽  
Xin Wang ◽  
Yanqiu Zhao ◽  
Xiaoxuan Ning ◽  
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2013 ◽  
Vol 30 (5) ◽  
pp. 2288-2296 ◽  
Author(s):  
ZONGLEI MAO ◽  
GUOCHUN BIAN ◽  
WEIHUA SHENG ◽  
SONGBIN HE ◽  
JICHENG YANG ◽  
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Phytomedicine ◽  
2020 ◽  
Vol 69 ◽  
pp. 153184 ◽  
Author(s):  
Mingming Deng ◽  
Bofang Liu ◽  
Huicong Song ◽  
Ruoxi Yu ◽  
Dan Zou ◽  
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2004 ◽  
Vol 3 (4) ◽  
pp. 377-381 ◽  
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Yumei Zhang ◽  
Yanqiu Zhao ◽  
Liu Hong ◽  
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Author(s):  
Tae Woo Kim

AbstractPrevious reports suggested that cinnamaldehyde (CA), the bioactive ingredient in Cinnamomum cassia, can suppress tumor growth, migratory, and invasive abilities. However, the role and molecular mechanisms of CA in GC are not completely understood. In the present study, we found that CA-induced ER stress and cell death via the PERK–CHOP axis and Ca2+ release in GC cells. Inhibition of ER stress using specific–siRNA blocked CA-induced cell death. Interestingly, CA treatment resulted in autophagic cell death by inducing Beclin-1, ATG5, and LC3B expression and by inhibiting p62 expression whereas autophagy inhibition suppressed CA-induced cell death. We showed that CA induces the inhibition of G9a and the activation of LC3B. Moreover, CA inhibited G9a binding on Beclin-1 and LC3B promoter. Overall, these results suggested that CA regulates the PERK–CHOP signaling, and G9a inhibition activates autophagic cell death via ER stress in GC cells.


2021 ◽  
Vol 21 (4) ◽  
Author(s):  
Qian Gu ◽  
Canhong Zhu ◽  
Xi Wu ◽  
Lianghuan Peng ◽  
Genya Huang ◽  
...  

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