Maternal embryonic leucine zipper kinase inhibits epithelial-mesenchymal transition by regulating transforming growth factor-β signaling

Cheng,Jianjian; Qin,Binyu; Liu,Bao; Huang,Taibo; Li,Yuguang; Ma,Lijun

doi:10.3892/ol.2017.6081

Maternal embryonic leucine zipper kinase inhibits epithelial-mesenchymal transition by regulating transforming growth factor-β signaling

Authors:
- Jianjian Cheng
- Binyu Qin
- Bao Liu
- Taibo Huang
- Yuguang Li
- Lijun Ma
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Affiliations: Department of Respiration and Critical Care and Emergency Medicine, Henan Provincial People's Hospital, Zhengzhou, Henan 450003, P.R. China
Published online on: April 24, 2017 https://doi.org/10.3892/ol.2017.6081
Pages: 4794-4798
Copyright: © Cheng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Maternal embryonic leucine zipper kinase (MELK) performs an important role in self‑renewal and proliferation of progenitor cells or tumor stem cells, and is expressed in aggressive cancers, contributing to tumorigenesis. However, the function of MELK in metastasis is unknown. In the present study, the lung cancer A549 cell line was utilized in order to study the role of MELK in epithelial-mesenchymal transitions (EMTs), the initial step of tumor metastasis. It was identified that transforming growth factor-β (TGF-β) could downregulate the expression of MELK, and that MELK could inhibit EMT by regulating TGF‑β signaling. MELK can interact with Smad proteins, which represses TGF‑β/Smad‑mediated signaling activity. The findings of the present study identified the effect of MELK in TGF‑β signaling and the EMT process.

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