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Cytokeratin 18 is necessary for initiation of TGF-β1-induced epithelial–mesenchymal transition in breast epithelial cells

Title
Cytokeratin 18 is necessary for initiation of TGF-β1-induced epithelial–mesenchymal transition in breast epithelial cells
Authors
Jung H.Kim B.Moon B.I.Oh E.-S.
Ewha Authors
문병인오억수
SCOPUS Author ID
문병인scopus; 오억수scopus
Issue Date
2016
Journal Title
Molecular and Cellular Biochemistry
ISSN
0300-8177JCR Link
Citation
vol. 423, no. 42737, pp. 21 - 28
Keywords
Breast cancerCytokeratin 18E-cadherinEpithelial–mesenchymal transitionSlug
Publisher
Springer New York LLC
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
During epithelial–mesenchymal transition (EMT), epithelial cells lose key phenotypic markers (e.g., E-cadherin and cytokeratin 18) and acquire mesenchymal markers (e.g., N-cadherin and vimentin). Although the loss of cytokeratin 18 is a hallmark of EMT, the regulatory role of cytokeratin 18 in EMT is not yet fully understood. Here, we report that cytokeratin 18 is involved in the regulation of transforming growth factor-beta1 (TGF-β1)-induced EMT in breast epithelial cells. When MCF10A cells were treated with TGF-β1 for 24 h, considerable morphological changes, indicative of the early stages of EMT (e.g., loss of cell–cell contact), were observed and cytokeratin 18 was downregulated. However, E-cadherin levels were not altered until a later time point. This suggests that cytokeratin 18 may play an active role during the earlier stages of EMT. Consistent with this notion, siRNA-mediated knockdown of cytokeratin 18 delayed TGF-β1-mediated EMT, and the associated downregulation of E-cadherin reduced the phosphorylation/nuclear localization of smad 2/3 and decreased the expression levels of snail and slug (which inhibit E-cadherin expression in epithelial cells as an early response to TGF-β1). Taken together, these results suggest that cytokeratin 18 critically contributes to initiating TGF-β1-induced EMT via the smad 2/3-mediated regulation of snail and slug expression in breast epithelial cells. © 2016, Springer Science+Business Media New York.
DOI
10.1007/s11010-016-2818-7
Appears in Collections:
의학전문대학원 > 의학과 > Journal papers
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