Cheng Jianjian, Qin Binyu, Liu Bao, Huang Taibo, Li Yuguang, Ma Lijun
Department of Respiration and Critical Care and Emergency Medicine, Henan Provincial People's Hospital, Zhengzhou, Henan 450003, P.R. China.
Oncol Lett. 2017 Jun;13(6):4794-4798. doi: 10.3892/ol.2017.6081. Epub 2017 Apr 24.
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.
母源胚胎亮氨酸拉链激酶（MELK）在祖细胞或肿瘤干细胞的自我更新和增殖中发挥重要作用，且在侵袭性癌症中表达，促进肿瘤发生。然而，MELK在转移中的功能尚不清楚。在本研究中，利用肺癌A549细胞系来研究MELK在肿瘤转移的起始步骤上皮-间质转化（EMT）中的作用。研究发现，转化生长因子-β（TGF-β）可下调MELK的表达，且MELK可通过调节TGF-β信号传导抑制EMT。MELK可与Smad蛋白相互作用，从而抑制TGF-β/Smad介导的信号活性。本研究结果明确了MELK在TGF-β信号传导和EMT过程中的作用。
