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Article type: Research Article
Authors: Lu, You-Zhua; b | Li, Yanga | Zhang, Tinga | Han, Shu-tanga; *
Affiliations: [a] Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China | [b] Digestive Department, The First Hospital of China Medical University, Shenyang, Liaoning, China
Correspondence: [*] Corresponding author: Shu-tang Han, Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210000, China. E-mail: 18941655039@163.com.
Abstract: Claudins are indispensible in modulating the permeability of epithelial and endothelial cells and in the maintenance of cell polarity. In order to verify the function of claudin-6 in the development of gastric cancer, we investigated claudin-6 expression in different gastric disease tissues. Moreover, we further explored whether overexpression of claudin-6 altered proliferation, apoptosis, migration, invasiveness, differentiation in BGC-823 cells and the potential mechanism. Immunohistochemistry was performed to detect the in situ expression of claudin-6 in different gastric disease tissues; moreover, cell culture, real-time PCR and western blot were used to evaluate the effect of overexpression of claudin-6 in vitro and the related mechanism. The results of immunohistochemical staining showed that the positivity of claudin-6 was significantly higher in superficial gastritis than that in gastric cancer. Overexpression of claudin-6 induced differentiation of BGC-823 cells by inhibiting the JNK pathway. However, it had no effect on proliferation, apoptosis, migration or invasiveness in vitro. The expression of claudin-6 was decreased in gastric cancer. Overexpression of claudin-6 induced differentiation of gastric cancer cells by inhibiting the JNK pathway.
Keywords: Gastric cancer, claudin-6, BGC-823, differentiation, JNK pathway
DOI: 10.3233/CBM-201554
Journal: Cancer Biomarkers, vol. 28, no. 3, pp. 329-340, 2020
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