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T-plastin contributes to epithelial-mesenchymal transition in human lung cancer cells through FAK/AKT/Slug axis signaling pathway

  • Soon Yong Park (Research Center, Dongnam Institute of Radiological & Medical Sciences) ;
  • Hyeongrok Choi (Department of Biomedical Sciences, Dong-A University) ;
  • Soo Min Choi (Department of Biomedical Sciences, Dong-A University) ;
  • Seungwon Wang (Department of Biomedical Sciences, Dong-A University) ;
  • Sangin Shim (Department of Agronomy, Gyeongsang National University) ;
  • Woojin Jun (Department of Food and Nutrition, Chonnam National University) ;
  • Jungkwan Lee (Department of Applied Biology, Dong-A University) ;
  • Jin Woong Chung (Department of Biomedical Sciences, Dong-A University)
  • Received : 2024.03.13
  • Accepted : 2024.04.26
  • Published : 2024.06.30

Abstract

T-plastin (PLST), a member of the actin-bundling protein family, plays crucial roles in cytoskeletal structure, regulation, and motility. Studies have shown that the plastin family is associated with the malignant characteristics of cancer, such as circulating tumor cells and metastasis, by inducing epithelial-mesenchymal transition (EMT) in various cancer cells. However, the role of PLST in the EMT of human lung cancer cells remains unclear. In this study, we observed that PLST overexpression enhanced cell migratory and invasive abilities, whereas its downregulation resulted in their suppression. Moreover, PLST expression levels were associated with the expression patterns of EMT markers, including E-cadherin, vimentin, and Slug. Furthermore, the phosphorylation levels of focal adhesion kinase (FAK) and AKT serine/threonine kinase (AKT) were dependent on PLST expression levels. These findings indicate that PLST induces the migration and invasion of human lung cancer cells by promoting Slug-mediated EMT via the FAK/AKT signaling pathway.

Keywords

Acknowledgement

This research was supported by the BB21plus funded by Busan Metropolitan City and Busan Techno Park.

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