Abstract | INTRODUCTION: MATERIAL AND METHODS: We determined the expression of BST2 in OSCC tissues using qRT-PCR, immunohistochemistry and western blot. Next, we used MTT assay, flow cytometry and western blot to determine the roles of BST2 in OSCC cell proliferation, cycle progression and apoptosis, respectively. Furthermore, we evaluated the effect of BST2 on gefitinib resistance in OSCC cells and explored the related molecular mechanism. RESULTS: BST2 expression was up-regulated in OSCC tissues compared with the adjacent normal tissues. BST2 overexpression significantly enhanced OSCC cell proliferation, mediated the cell cycle progression and inhibited cell apoptosis. Additionally, the results showed that BST2 overexpression effectively induced gefitinib resistance in OSCC cells. Subsequent analysis revealed that the underlying mechanism was associated with activation of the EGFR pathway. CONCLUSIONS: Our study indicated that BST2 promoted growth and induced gefitinib resistance in OSCC cells, at least partially, through regulating the EGFR pathway. Thus, BST2 could be used as a therapeutic target for gefitinib resistance in OSCC.
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Authors | Huang Jin, Lianping Zhang, Shufang Wang, Lei Qian |
Journal | Archives of medical science : AMS
(Arch Med Sci)
Vol. 17
Issue 6
Pg. 1772-1782
( 2021)
ISSN: 1734-1922 [Print] Poland |
PMID | 34900059
(Publication Type: Journal Article)
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Copyright | Copyright: © 2019 Termedia & Banach. |