Open AccessBST2 promotes growth and induces gefitinib resistance in oral squamous cell carcinoma via regulating the EGFR pathway
Author(s) -
Jin Huang,
Lianping Zhang,
Shufang Wang,
Lei Qian
Publication year - 2019
Publication title -
archives of medical science/archives of medical science (online)
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 46
eISSN - 1896-9151
pISSN - 1734-1922
DOI - 10.5114/aoms.2019.86183
Subject(s) - gefitinib , cancer research , cell growth , apoptosis , cell cycle , cell , western blot , medicine , flow cytometry , cancer , biology , immunology , epidermal growth factor receptor , gene , biochemistry
Gefitinib, well known as a new antitumor agent, has been applied in various cancers such as oral squamous cell carcinoma (OSCC). However, most patients eventually acquire resistance to gefitinib, and the molecular mechanism of gefitinib resistance is not well described. Bone marrow stromal cell antigen 2 (BST2) has been reported to promote tumor cell growth and confer chemotherapy resistance in various cancers. However, the roles of BST2 in OSCC still need to be fully understood. 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.