Research Paper|Volume 13, Issue 9|pp 13048—13060

Ectopic expression of MELK in oral squamous cell carcinoma and its correlation with epithelial mesenchymal transition

Bo Li¹, Xinghuanyu Xu¹, Xin Bin¹, Jiang Zhou¹, Zhangui Tang¹

¹Xiangya School of Stomatology, Central South University, Changsha, Hunan 410008, PR China

Received: October 1, 2020Accepted: March 23, 2021Published: May 7, 2021

https://doi.org/10.18632/aging.202986

Copyright: © 2021 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Epithelial–mesenchymal transition (EMT) is closely correlated to metastasis formation generation and maintenance of cancer stem cells, nevertheless, the underlying mechanisms are unclear. The aim of this study is to investigate the role of maternal embryonic leucine-zipper kinase (MELK) in EMT regulation in oral squamous cell carcinoma (OSCC). We found that there was overexpression of MELK in human OSCC tissues, and high MELK expression was correlated with lymphatic metastasis and led to poor prognosis in patients with OSCC. We also confirmed that MELK is closely correlated to the EMT process using a human OSCC tissue microarray. Additionally, MELK expression was observed to be regulated in several OSCC cell lines, and knockdown of MELK genes inhibited cell proliferation, migration, invasion and EMT of OSCC cells in vitro. Furthermore, silencing of MELK suppressed tumour growth in vivo, and experimental research verified that MELK may augment OSCC development via mediating the Wnt/Notch signalling pathway. Our findings suggest that MELK serves as an oncogene to improve malignant development of OSCC via enhancing EMT, and MELK might be a potential target for anticancer therapeutic.