scholarly journals Expression and biological role of DKK1 in human esophageal cancer

2011 ◽  
Vol 19 (20) ◽  
pp. 2116
Author(s):  
Shu-Jun Li ◽  
Yu-Zheng He ◽  
Bao-Lei Lv ◽  
Xiu-Lan Niu ◽  
Ai-Rong Cui ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Biological Role ◽  
Human Esophageal Cancer

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.

Toxicity and Role of Fumonisins in Animal Diseases and Human Esophageal Cancer

1994 ◽  
Vol 57 (6) ◽  
pp. 522-527 ◽  
Author(s):  
WILLIAM P. NORRED ◽  
KENNETH A. VOSS
Keyword(s):  
Esophageal Cancer ◽  
Fusarium Proliferatum ◽  
Brain Lesions ◽  
Lung Edema ◽  
Laboratory Rats ◽  
The World ◽  
Causative Agents ◽  
Human Esophageal Cancer ◽  
Action Levels

Fumonisins are secondary metabolites of Fusarium moniliforme, Fusarium proliferatum and several other Fusaria that commonly contaminate corn. Only recently discovered in 1988, these mycotoxins appear to be the causative agents of several toxicoses in animals that result from ingestion of moldy corn or corn-based feeds. The syndromes observed vary considerably among the different species affected and include brain lesions in equids, lung edema in swine, and nephrotoxicity, hepatotoxicity and hepatocellular carcinoma in laboratory rats. There is also evidence that suggests that F. moniliforme and fumonisins may also be responsible for esophageal cancer in humans in certain areas of the world where moldy corn is frequently consumed. Studies are currently underway to determine the extent of the hazards posed by fumonisins, and whether controls in the form of regulatory action levels may be necessary.

scholarly journals PD-L1 Expression Promotes Epithelial to Mesenchymal Transition in Human Esophageal Cancer

2017 ◽  
Vol 42 (6) ◽  
pp. 2267-2280 ◽  
Author(s):  
Lujun Chen ◽  
Yuqi Xiong ◽  
Jing Li ◽  
Xiao Zheng ◽  
Qi Zhou ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Cancer Immunotherapy ◽  
Cancer Cell ◽  
Epithelial To Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Esophageal Cancer Cell ◽  
Human Esophageal Cancer ◽  
Cancer Tissues

Background/Aims: PD-L1 (Programmed cell death 1 ligand 1, PD-L1), an essential immune checkpoint molecule in the tumor microenvironment, is an important target for cancer immunotherapy. We have previously reported that its expression in human gastric and esophageal cancer tissues is significantly associated with cancer progression and patients’ postoperative prognoses. Its expression in cancer cells is well known to inhibit the T cell-mediated anti-tumor response, and this mechanism of action has been targeted for cancer immunotherapy. As of now, the autonomous effect of PD-L1 on cancer cells is not well understood, thus our present study aimed to examine the role of PD-L1 intervention in cellular biological functions, especially epithelial to mesenchymal transition (EMT), of the human esophageal cancer cell line, Eca-109 cells. Methods: Immunohistochemistry assay was used to investigate the correlation between expression of PD-L1 and EMT markers in human esophageal cancer tissues. Intervention of PD-L1 by using RNAi and over-expression methods were used to study the role of PD-L1 in regulation of biological behaviors and EMT in Eca-109 cells. Results: Our clinical and pathological data demonstrated that tumor samples in the EMT positive subgroup had higher PD-L1 expression than those in the EMT negative subgroup. By manipulating PD-L1 expression in Eca-109 cells either through ablation or overexpression of wild type and the cytoplasmic domain-truncated mutant, we demonstrated that PD-L1 expression significantly promoted the cell viability, migration and EMT phenotype. Furthermore, our study also indicated that PD-1 fusion protein mediated stimulation of PD-L1 and the cytoplasmic domain of PD-L1 played a critical role in promoting EMT phenotype of Eca-109 cells, thereby suggesting that PD-1 receptor usually by triggering the reverse signaling can effect PD-L1 mediated regulation of esophageal cancer cell response. Conclusion: Our present study reveals a tumor cell-autonomous role of PD-L1 signaling in promoting EMT in human esophageal cancer.

THE ROLE OF BRACHYTHERAPY IN TREATMENT FOR ESOPHAGEAL CANCER

2017 ◽  
Vol 63 (4) ◽  
pp. 660-665
Author(s):  
Yelena Tyuryaeva
Keyword(s):  
Esophageal Cancer ◽  
Critical Review ◽  
Palliative Treatment ◽  
Combined Treatment ◽  
Neoadjuvant Treatment ◽  
Early Esophageal Cancer ◽  
Separate Section ◽  
Treatment Regimens ◽  
Contradictory Data

The article is devoted to various aspects of the use of intraluminal brachytherapy (IB) in treatment for esophageal cancer (EC). A critical review of the use of IB as a component of combined radiotherapy/chemoradiotherapy in neoadjuvant treatment regimens, for definitive CRT, as well as in palliative treatment of non-operable tumors of this localization is given. The contradictory data on the effectiveness of brachytherapy with locally distributed, inoperable EC are summarized. A separate section relates to the prospects for incorporating brachytherapy into combined treatment of early esophageal cancer. Carried out analysis testifies to the necessity of standardization of summary and daily doses of irradiation depending on the indications to the IB.

Methylation of ZNF331 Promotes Cell Invasion and Migration in Human Esophageal Cancer

2015 ◽  
Vol 16 (4) ◽  
pp. 322-328 ◽  
Author(s):  
Suzhen Jiang ◽  
Enqiang Linghu ◽  
Qimin Zhan ◽  
Weidong Han ◽  
Mingzhou Guo
Keyword(s):  
Esophageal Cancer ◽  
Cell Invasion ◽  
Invasion And Migration ◽  
And Migration ◽  
Human Esophageal Cancer

From Organizations of Processes to Organisms and Other Biological Individuals

2018 ◽  
Author(s):  
Argyris Arnellos
Keyword(s):  
Multicellular Organism ◽  
Collaborative Networks ◽  
Biological Role ◽  
Regulatory Processes ◽  
Different Types ◽  
Organizational Framework

The emphasis on the collaborative dimension of life overlooks the importance of biological individuals (conceived of as integrated, self-maintaining organizations) in the build-up of more complex collaborative networks in the course of evolution. This chapter proposes a process-based organizational ontology for biology, according to which the essential features of unicellular organismicality are captured by a self-maintaining organization of processes integrated by means of a special type of collaboration (realized through regulatory processes entailing an indispensable interdependence) between its constitutive and its interactive aspects. This ontology is then used to describe different types of collaborations among cells and to suggest the type that yields a multicellular organism. The proposed organizational framework enables us to critically assess hypercollaborative views of life, especially issues related to the distinction between biological individuals and organisms and between life and non-life, without however underestimating the central biological role of collaboration.

scholarly journals Tocopherols and Tocotrienols—Bioactive Dietary Compounds; What Is Certain, What Is Doubt?

2021 ◽  
Vol 22 (12) ◽  
pp. 6222
Author(s):  
Kacper Szewczyk ◽  
Aleksandra Chojnacka ◽  
Magdalena Górnicka
Keyword(s):  
Vitamin E ◽  
Metabolic Disorders ◽  
Tissue Concentration ◽  
Biological Properties ◽  
Biological Role ◽  
Future Research ◽  
The Past ◽  
The Subject ◽  
The Relationship

Tocopherols and tocotrienols are natural compounds of plant origin, available in the nature. They are supplied in various amounts in a diet, mainly from vegetable oils, some oilseeds, and nuts. The main forms in the diet are α- and γ-tocopherol, due to the highest content in food products. Nevertheless, α-tocopherol is the main form of vitamin E with the highest tissue concentration. The α- forms of both tocopherols and tocotrienols are considered as the most metabolically active. Currently, research results indicate also a greater antioxidant potential of tocotrienols than tocopherols. Moreover, the biological role of vitamin E metabolites have received increasing interest. The aim of this review is to update the knowledge of tocopherol and tocotrienol bioactivity, with a particular focus on their bioavailability, distribution, and metabolism determinants in humans. Almost one hundred years after the start of research on α-tocopherol, its biological properties are still under investigation. For several decades, researchers’ interest in the biological importance of other forms of vitamin E has also been growing. Some of the functions, for instance the antioxidant functions of α- and γ-tocopherols, have been confirmed in humans, while others, such as the relationship with metabolic disorders, are still under investigation. Some studies, which analyzed the biological role and mechanisms of tocopherols and tocotrienols over the past few years described new and even unexpected cellular and molecular properties that will be the subject of future research.

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