Journal
INTERNATIONAL JOURNAL OF ONCOLOGY
Volume 45, Issue 4, Pages 1515-1522Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/ijo.2014.2554
Keywords
ezrin; epithelial-mesenchymal transition; actin filament reorganization; cell metastasis; podocalyxin
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Funding
- National Program on Key Basic Research Project (973 Program) [2011CB910700]
- High-Level Talents Project of the Universities of Guangdong [[2011]431]
- National Natural Science Foundation of China [31000628]
- Fundamental Research Funds for the Central Universities [21611430, 21610101, 21609317]
- Natural Science Foundation of Guangdong Province [S2013030013315]
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Epithelial mesenchymal transition (EMT) has been shown to play a role in cellular differentiation during development and tumor invasion. However, the precise molecular mechanisms of EMT are not fully elucidated. Previous studies suggested that the mechanism underlying the possible involvement of ezrin in EMT process might be different from that of moesin, another ERM protein. In our study, we examined the role of ezrin in actin filament reorganization and cell metastasis during TGF-beta 1-induced alveolar EMT. Suppressing ezrin expression limited morphological changes and actin filament remodeling, decreased cell migration and invasion during EMT. Immunofluorescence experiments indicated that EMT characteristics in lung cancer cells are associated to differential ezrin subcellular localization. We also found that podocalyxin interacted with ezrin after TGF-beta 1 induction. Therefore, ezrin is an important regulator of the EMT process, and its function might possibly be mediated by the ezrin-podocalyxin interaction during TGF-beta 1-induced alveolar EMT. Our finding provides important new insights into the mechanisms of action of the ERM proteins in the TGF-beta 1-induced alveolar EMT.
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