Abstract | BACKGROUND:
Oral cancer metastasis is a devastating process that contributes to poor prognosis and high mortality, yet its detailed underlying mechanisms remain unclear. Here, we aimed to evaluate metastasis-specific markers in oral cancer and to provide comprehensive recognition concerning functional roles of the specific target in oral cancer metastasis. METHODS: RESULTS:
LGALS1 was observed to be upregulated in highly invasive oral cancer cells, and elevated LGALS1 expression was correlated with cancer progression and lymph node metastasis in oral cancer tissue specimens. Functionally, silencing LGALS1 resulted in suppressed cell growth, wound healing, cell migration, and cell invasion in oral cancer cells in vitro. Knockdown of LGALS1 in highly invasive oral cancer cells dramatically inhibited lung metastasis in an in vivo mouse model. Mechanistic studies suggested p38 mitogen-activated protein kinase (MAPK) phosphorylation, upregulated MMP-9, and mesenchymal phenotypes of epithelial-mesenchymal transition (EMT) in highly invasive oral cancer cells, whereas siRNA against LGALS1 resulted in the inactivation of p38 MAPK pathway, downregulated MMP-9, and EMT inhibition. CONCLUSIONS:
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Authors | Ji-Min Li, Chien-Wei Tseng, Chi-Chen Lin, Ching-Hsuan Law, Yu-An Chien, Wen-Hung Kuo, Hsiu-Chuan Chou, Wen-Ching Wang, Hong-Lin Chan |
Journal | Therapeutic advances in medical oncology
(Ther Adv Med Oncol)
Vol. 10
Pg. 1758835918794622
( 2018)
ISSN: 1758-8340 [Print] England |
PMID | 30159048
(Publication Type: Journal Article)
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