The expression of the tumor suppressor gene connexin 26 is not mediated by methylation in human esophageal cancer cells

2003 ◽  
Vol 36 (2) ◽  
pp. 74-81 ◽  
Author(s):  
Jadranka Loncarek ◽  
Hiroshi Yamasaki ◽  
Pierre Levillain ◽  
Serge Milinkevitch ◽  
Marc Mesnil
Keyword(s):  
Esophageal Cancer ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Tumor Suppressor Gene ◽  
Suppressor Gene ◽  
Connexin 26 ◽  
Human Esophageal Cancer ◽  
Esophageal Cancer Cells

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 Induction of PDCD4 tumor suppressor gene expression by RAR agonists, antiestrogen and HER-2/neu antagonist in breast cancer cells. Evidence for a role in apoptosis

Oncogene ◽  
2004 ◽  
Vol 23 (49) ◽  
pp. 8135-8145 ◽  
Author(s):  
Olubunmi Afonja ◽  
Dominique Juste ◽  
Sharmistha Das ◽  
Sachiko Matsuhashi ◽  
Herbert H Samuels
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Tumor Suppressor Gene ◽  
Breast Cancer Cells ◽  
Suppressor Gene ◽  
Her 2

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 A High-Throughput Screen with Isogenic PTEN+/+ and PTEN−/− Cells Identifies CID1340132 as a Novel Compound That Induces Apoptosis in PTEN and PIK3CA Mutant Human Cancer Cells

2011 ◽  
Vol 16 (4) ◽  
pp. 383-393 ◽  
Author(s):  
Hui-Fang Li ◽  
Adam Keeton ◽  
Michele Vitolo ◽  
Clinton Maddox ◽  
Lynn Rasmussen ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Cancer Cells ◽  
Tumor Suppressor Gene ◽  
High Throughput ◽  
Human Cancer ◽  
Genetic Difference ◽  
Suppressor Gene ◽  
Pten Gene ◽  
Target Cells ◽  
Mutant Cells

The PTEN tumor suppressor gene is one of the most commonly mutated genes in human cancer. Because inactivation of PTEN is a somatic event, PTEN mutations represent an important genetic difference between cancer cells and normal cells and therefore a potential anticancer drug target. However, it remains a substantial challenge to identify compounds that target loss-of-function events such as mutations of tumor suppressors. In an effort to identify small molecules that preferentially kill cells with mutations of PTEN, the authors developed and implemented a high-throughput, paired cell-based screen composed of parental HCT116 cells and their PTEN gene-targeted derivatives. From 138 758 compounds tested, two hits were identified, and one, N′-[(1-benzyl-1H-indol-3-yl)methylene]benzenesulfonohydrazide (CID1340132), was further studied using a variety of cell-based models, including HCT116, MCF10A, and HEC1A cells with targeted deletion of either their PTEN or PIK3CA genes. Preferential killing of PTEN and PIK3CA mutant cells was accompanied by DNA damage, inhibition of DNA synthesis, and apoptosis. Taken together, these data validate a cell-based screening approach for identifying lead compounds that target cells with specific tumor suppressor gene mutations and describe a novel compound with preferential killing activity toward PTEN and PIK3CA mutant cells.

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