scholarly journals miR302a inhibits the proliferation of esophageal cancer cells through the MAPK and PI3K/Akt signaling pathways

2018 ◽  
Author(s):  
Daokui Xia ◽  
Shumei Tian ◽  
Zhen Chen ◽  
Wenchao Qin ◽  
Quan Liu
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Akt Signaling ◽  
Esophageal Cancer Cells

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 ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Vitamin E ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Akt Signaling ◽  
Vitamin E Succinate ◽  
Esophageal Cancer Cells

scholarly journals Cordycepin enhances the chemosensitivity of esophageal cancer cells to cisplatin by inducing the activation of AMPK and suppressing the AKT signaling pathway

2020 ◽  
Vol 11 (10) ◽  
Author(s):  
Ying Gao ◽  
Dan-Lei Chen ◽  
Mi Zhou ◽  
Zhou-san Zheng ◽  
Mei-Fang He ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Combination Therapy ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Caspase 3 ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Expression Levels ◽  
In Vivo Animal Model ◽  
Esophageal Cancer Cells

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.

scholarly journals Plumbagin inhibits the proliferation and survival of esophageal cancer cells by blocking STAT3-PLK1-AKT signaling

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

TNF-α-induced IL-32 expression in esophageal cancer: cross talk JNK/Akt signaling pathways

2013 ◽  
Vol 1 (2) ◽  
pp. 73-85 ◽  
Author(s):  
Jack Neuzillet ◽  
Cailin Traynor ◽  
Grace Hullmann ◽  
Gabriel Tyritzis ◽  
John Shimizu
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Inflammatory Diseases ◽  
Enzyme Linked Immunosorbent Assay ◽  
Potential Marker ◽  
Tnf Α ◽  
Autoimmune And Inflammatory Diseases ◽  
Human Esophageal Cancer ◽  
Esophageal Cancer Cells

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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