scholarly journals Vitamin E succinate induces apoptosis via the PI3K/AKT signaling pathways in EC109 esophageal cancer cells

2016 ◽  
Vol 14 (2) ◽  
pp. 1531-1537 ◽  
Author(s):  
Peng Yang ◽  
Jiaying Zhao ◽  
Liying Hou ◽  
Lei Yang ◽  
Kun Wu ◽  
...  
2020 ◽  
Vol 11 (10) ◽  
Author(s):  
Ying Gao ◽  
Dan-Lei Chen ◽  
Mi Zhou ◽  
Zhou-san Zheng ◽  
Mei-Fang He ◽  
...  

Abstract Although cisplatin (cDDP), is a first-line chemotherapy drug for esophageal cancer, it still has the potential to develop drug resistance and side effects. There is increasing evidence that cordycepin can work synergistically with other chemotherapy drugs. Therefore, we investigated whether combination therapy of cordycepin and cDDP may enhance the therapeutic effect of cDDP. We performed a series of functional tests to study the effect of medical treatment on esophageal cancer cells. We then used GO analysis to examine the pathways affected by treatment with cordycepin and cDDP. Next, we observed changes in the abundance of the selected pathway proteins. The in vivo animal model supported the results of the in vitro experiments. Co-treatment with cordycepin and cDDP inhibited cell growth, migration, and metastasis, as well as induced apoptosis. Cordycepin was found to effectively enhance activation of AMPK and inhibited activity of AKT. In all treatment groups, the expression levels of p-PI3K, p-Akt, p-p70S6K, Caspase-3, and Bcl-2 were significantly reduced, while the expression levels of p-AMPK, cleaved Caspase-3, and Bax increased, and the total levels of Akt, PI3K, and p70S6K levels remained unchanged. Overall, cordycepin was found to enhance the chemical sensitivity of esophageal cancer cells to cisplatin by inducing AMPK activation and inhibiting the AKT signaling pathway. Combination therapy of cordycepin and cisplatin represent a novel potential treatment of esophageal cancer.


2018 ◽  
Vol 9 (2) ◽  
Author(s):  
Ying-Ya Cao ◽  
Jing Yu ◽  
Ting-Ting Liu ◽  
Kai-Xia Yang ◽  
Li-Yan Yang ◽  
...  

2013 ◽  
Vol 1 (2) ◽  
pp. 73-85 ◽  
Author(s):  
Jack Neuzillet ◽  
Cailin Traynor ◽  
Grace Hullmann ◽  
Gabriel Tyritzis ◽  
John Shimizu

Esophageal cancer is the seventh leading cause of cancer death in males in USA, Interleukin (IL)-32 is a recently identified proinflammatory cytokine that is one of the IL-18 inducible genes, and plays an important role in autoimmune and inflammatory diseases. IL-32 is recently described in esophageal cancer pathway via induction of nuclear factor NF-κB activation. We investigated the expression of IL-32 by TNF-α in esophageal cancer. Human esophageal cancer cells were cultured in the presence or absence of TNF-α to analyze the expression of IL-32 by quantitative RT-PCR and enzyme-linked immunosorbent assay. Further, activation of Akt and JNK signaling pathways were investigated by Western blot. TNF-α induced enhanced IL-32 release in human esophageal cancer cells. These data suggest that activation of Akt and JNK pathways regulated TNF-α-induced IL-32 expression in human esophageal cancer. We concluded that TNF-α/IL-32 pathway may be a potential marker and may be therapeutic target for esophageal cancer.


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