scholarly journals Pterostilbene Inhibits the Growth of Human Esophageal Cancer Cells by Regulating Endoplasmic Reticulum Stress

2016 ◽  
Vol 38 (3) ◽  
pp. 1226-1244 ◽  
Author(s):  
Yingtong Feng ◽  
Yang Yang ◽  
Chongxi Fan ◽  
Shouyin Di ◽  
Wei Hu ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Esophageal Cancer ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Apoptotic Index ◽  
Related Protein ◽  
Apoptosis Related Protein ◽  
Human Esophageal Cancer ◽  
Esophageal Cancer Cells

Background/Aims: Pterostilbene (PTE), a natural dimethylated resveratrol analog from blueberries, is known to have diverse pharmacological activities, including anticancer properties. In this study, we investigated the anticancer activity of PTE against human esophageal cancer cells both in vitro and in vivo and explored the role of endoplasmic reticulum (ER) stress (ERS) signaling in this process. Methods: Cell viability, the apoptotic index, Caspase 3 activity, adhesion, migration, reactive oxygen species (ROS) levels, and glutathione (GSH) levels were detected to explore the effect of PTE on human EC109 esophageal cancer cells. Furthermore, siRNA transfection and a chemical inhibitor were employed to confirm the role of ERS. Results: PTE treatment dose- and time-dependently decreased the viability of human esophageal cancer EC109 cells. PTE also decreased tumor cell adhesion, migration and intracellular GSH levels while increasing the apoptotic index, Caspase 3 activity and ROS levels, which suggest the strong anticancer activity of PTE. Furthermore, PTE treatment increased the expression of ERS-related molecules (GRP78, ATF6, p-PERK, p-eIF2α and CHOP), upregulated the pro-apoptosis-related protein PUMA and downregulated the anti-apoptosis-related protein Bcl-2 while promoting the translocation of cytochrome c from mitochondria to cytosol and the activation of Caspase 9 and Caspase 12. The downregulation of ERS signaling by CHOP siRNA desensitized esophageal cancer cells to PTE treatment, whereas upregulation of ERS signaling by thapsigargin (THA) had the opposite effect. N-Acetylcysteine (NAC), a ROS scavenger, also desensitized esophageal cancer cells to PTE treatment. Conclusions: Overall, the results indicate that PTE is a potent anti-cancer pharmaceutical against human esophageal cancer, and the possible mechanism involves the activation of ERS signaling pathways.

scholarly journals Characteristics of P-Type and N-Type Photoelectrochemical Biosensors: A Case Study for Esophageal Cancer Detection

Nanomaterials ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 1065
Author(s):  
Joseph-Hang Leung ◽  
Hong-Thai Nguyen ◽  
Shih-Wei Feng ◽  
Sofya B. Artemkina ◽  
Vladimir E. Fedorov ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Carrier Transport ◽  
X Ray Diffraction ◽  
Photoelectrochemical Response ◽  
Carrier Separation ◽  
Human Esophageal Cancer ◽  
P Type ◽  
Esophageal Cancer Cells

P-type and N-type photoelectrochemical (PEC) biosensors were established in the laboratory to discuss the correlation between characteristic substances and photoactive material properties through the photogenerated charge carrier transport mechanism. Four types of human esophageal cancer cells (ECCs) were analyzed without requiring additional bias voltage. Photoelectrical characteristics were examined by scanning electron microscopy (SEM), X-ray diffraction (XRD), UV–vis reflectance spectroscopy, and photocurrent response analyses. Results showed that smaller photocurrent was measured in cases with advanced cancer stages. Glutathione (L-glutathione reduced, GSH) and Glutathione disulfide (GSSG) in cancer cells carry out redox reactions during carrier separation, which changes the photocurrent. The sensor can identify ECC stages with a certain level of photoelectrochemical response. The detection error can be optimized by adjusting the number of cells, and the detection time of about 5 min allowed repeated measurement.

scholarly journals PSMD4 regulates the malignancy of esophageal cancer cells by suppressing endoplasmic reticulum stress

2019 ◽  
Vol 35 (10) ◽  
pp. 591-597 ◽  
Author(s):  
Ai‐Guo Ma ◽  
Li‐Mei Yu ◽  
Hong Zhao ◽  
Cun‐Wei Qin ◽  
Xiang‐Yu Tian ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Esophageal Cancer ◽  
Endoplasmic Reticulum Stress ◽  
Cancer Cells ◽  
Esophageal Cancer Cells

Bioactivities of Sophorolipid with Different Structures Against Human Esophageal Cancer Cells

2012 ◽  
Vol 173 (2) ◽  
pp. 286-291 ◽  
Author(s):  
Lingjian Shao ◽  
Xin Song ◽  
Xiaojing Ma ◽  
Hui Li ◽  
Yinbo Qu
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Human Esophageal Cancer ◽  
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.

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