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Ectopic expression of MELK in oral squamous cell carcinoma and its correlation with epithelial mesenchymal transition
- Source :
- Aging (Albany NY)
- Publication Year :
- 2021
- Publisher :
- Impact Journals, LLC, 2021.
-
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.
- Subjects :
- Aging
Protein Serine-Threonine Kinases
Biology
Ectopic Gene Expression
Cell Movement
Cancer stem cell
MELK
Humans
Gene silencing
Epithelial–mesenchymal transition
Cell Proliferation
Tissue microarray
Oncogene
Squamous Cell Carcinoma of Head and Neck
Cell growth
EMT
Wnt signaling pathway
Cell Biology
stomatognathic diseases
Head and Neck Neoplasms
Lymphatic Metastasis
Carcinoma, Squamous Cell
Neoplastic Stem Cells
Cancer research
Mouth Neoplasms
Ectopic expression
OSCC
Research Paper
Subjects
Details
- ISSN :
- 19454589
- Volume :
- 13
- Database :
- OpenAIRE
- Journal :
- Aging
- Accession number :
- edsair.doi.dedup.....55fbf608bc5f0abf5ee6702356464164