miR-200c-141 induces a hybrid E/M state and promotes collective cell migration in MDA-MB-231 cells.

Autor: Nagai T; Department of Biochemistry, Fukushima Medical University, School of Medicine, Fukushima, 960-1295, Japan. Electronic address: tnagai@fmu.ac.jp., Sato M; Department of Biochemistry, Fukushima Medical University, School of Medicine, Fukushima, 960-1295, Japan., Nishita M; Department of Biochemistry, Fukushima Medical University, School of Medicine, Fukushima, 960-1295, Japan. Electronic address: nishita@fmu.ac.jp.
Jazyk: angličtina
Zdroj: Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2024 May 21; Vol. 709, pp. 149829. Date of Electronic Publication: 2024 Mar 26.
DOI: 10.1016/j.bbrc.2024.149829
Abstrakt: The microRNA-200 (miR-200) family is a potent suppressor of epithelial-to-mesenchymal transition (EMT). While its role as a tumor suppressor has been well documented, recent studies suggested that it can promote cancer progression in several stages. In this study, we investigated whether the miR-200 family members play a role in the acquisition of a hybrid epithelial/mesenchymal (E/M) state, which is reported to be associated with cancer malignancy, in mesenchymal MDA-MB-231 cells. Our results demonstrated that the induction of miR-200c-141, a cluster of the miR-200 family member, can induce the expression of epithelial gene and cell-cell junction while mesenchymal markers are retained. Moreover, induction of miR-200c-141 promoted collective migration accompanied by the formation of F-actin cables anchored by adherens junction. These results suggest that the miR-200 family can induce a hybrid E/M state and endows with the ability of collective cell migration in mesenchymal cancer cells.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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