Abstract

Abstract Claudin-1 (CLDN1) is overexpressed in gastric cancer and correlated with tumor invasion, metastasis and poor outcome. Here, we both down and up regulated CLDN1 expression in gastric cancer cells to elucidate its role in gastric carcinogenesis and tumor progression. As results, we found that deficiency of CLDN1 inhibited cells migration, invasion, and colony formation in vitro and tumorigenicity, metastasis in vivo. Furthermore, CLDN1 expression promoted cell aggregation and increased anoikis resistance. Down or up regulated CLDN1 were accompanied with variations of membrane β-catenin expression and activities of Akt and Src signals. When β-catenin was up-regulated in CLDN1-KD cell, cell aggregation and anoikis resistance were restored, and Akt and Src signal pathways were re-activated. Taken together, these findings suggested that CLDN1 may function as an oncogene in gastric cancer and its malignant potential may attribute to the regulation of cell anoikis through mediating membrane β-catenin regulated cell-cell adhesion and survival signals of Akt and Src. Note: This abstract was not presented at the meeting. Citation Format: Jiangfang Li, Jie Huang, Bingya Liu, Zhenggang Zhu. Claudin-1 enhances tumor proliferation and metastasis by regulating cell anoikisin gastric cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 5197. doi:10.1158/1538-7445.AM2015-5197

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