Abstract

Abstract Epithelial-mesenchymal transition or transformation (EMT) is a process characterized by loss of cell adhesion, repression of E-cadherin expression, and increased cell motility. Epithelial-mesenchymal transition (EMT) confers tumor cells with metastatic dissemination, cancer stem cell-like characters and drug resistance. However, the molecular mechanism for metastatic dissemination remains unclear. Initiation of metastasis involves invasion, which has many phenotypic similarities to EMT, including a loss of cell-cell adhesion mediated by E-cadherin repression and an increase in cell mobility. In this study, we induced EMT in colon cancer cell line LoVo with expression of Twist, a key transcriptional factor of EMT. The metastasis associated with EMT was determined E-cadherin, vimentin and β-catenin protein expression by western blot and morphological changes associated with EMT in these cells. We found that expression of Twist induced a morphological change associated with EMT in these cells. We also found that the E-cadherin was significantly decreased in Twist-overexpressing cells LoVo. Interestingly, we showed that β-catenin was activated in these Twist-overexpressing cells. Our results indicate that activation of β-catenin is required for the sustention of EMT-associated metastasis dissemination. Citation Format: Hye Ryeon Kim, SoYoung Kim, Young Ae Baik, Hye Kyung Hong, Woo Yong Lee, Yong Beom Cho. Role of Twist for maintenance of EMT in colon cancer cell . [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1499. doi:10.1158/1538-7445.AM2013-1499

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