T-plastin contributes to epithelial-mesenchymal transition in human lung cancer cells through FAK/AKT/Slug axis signaling pathway
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T-plastin (PLST), a member of the actin-bundling protein family,plays crucial roles in cytoskeletal structure, regulation, andmotility. Studies have shown that the plastin family is associatedwith the malignant characteristics of cancer, such ascirculating tumor cells and metastasis, by inducing epithelialmesenchymaltransition (EMT) in various cancer cells. However,the role of PLST in the EMT of human lung cancer cells remainsunclear. In this study, we observed that PLST overexpressionenhanced cell migratory and invasive abilities, whereasits downregulation resulted in their suppression. Moreover, PLSTexpression levels were associated with the expression patternsof EMT markers, including E-cadherin, vimentin, and Slug. Furthermore,the phosphorylation levels of focal adhesion kinase(FAK) and AKT serine/threonine kinase (AKT) were dependenton PLST expression levels. These findings indicate that PLSTinduces the migration and invasion of human lung cancer cellsby promoting Slug-mediated EMT via the FAK/AKT signalingpathway.
Abstract
T-plastin (PLST), a member of the actin-bundling protein family,plays crucial roles in cytoskeletal structure, regulation, andmotility. Studies have shown that the plastin family is associatedwith the malignant characteristics of cancer, such ascirculating tumor cells and metastasis, by inducing epithelialmesenchymaltransition (EMT) in various cancer cells. However,the role of PLST in the EMT of human lung cancer cells remainsunclear. In this study, we observed that PLST overexpressionenhanced cell migratory and invasive abilities, whereasits downregulation resulted in their suppression. Moreover, PLSTexpression levels were associated with the expression patternsof EMT markers, including E-cadherin, vimentin, and Slug. Furthermore,the phosphorylation levels of focal adhesion kinase(FAK) and AKT serine/threonine kinase (AKT) were dependenton PLST expression levels. These findings indicate that PLSTinduces the migration and invasion of human lung cancer cellsby promoting Slug-mediated EMT via the FAK/AKT signalingpathway.
참고문헌 (38)
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