BST2 promotes growth and induces gefitinib resistance in oral squamous cell carcinoma via regulating the EGFR pathway
Introduction 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 stro...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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Termedia Publishing House
2019-07-01
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| Series: | Archives of Medical Science |
| Subjects: | |
| Online Access: | https://www.archivesofmedicalscience.com/BST2-promotes-growth-and-induces-gefitinib-resistance-in-oral-squamous-cell-carcinoma,108624,0,2.html |
| _version_ | 1811181225675587584 |
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| author | Huang Jin Lianping Zhang Shufang Wang Lei Qian |
| author_facet | Huang Jin Lianping Zhang Shufang Wang Lei Qian |
| author_sort | Huang Jin |
| collection | DOAJ |
| description | Introduction
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. |
| first_indexed | 2024-04-11T09:15:24Z |
| format | Article |
| id | doaj.art-d6e98cb4186546b195ff09826209d7aa |
| institution | Directory Open Access Journal |
| issn | 1734-1922 1896-9151 |
| language | English |
| last_indexed | 2024-04-11T09:15:24Z |
| publishDate | 2019-07-01 |
| publisher | Termedia Publishing House |
| record_format | Article |
| series | Archives of Medical Science |
| spelling | doaj.art-d6e98cb4186546b195ff09826209d7aa2022-12-22T04:32:23ZengTermedia Publishing HouseArchives of Medical Science1734-19221896-91512019-07-011761772178210.5114/aoms.2019.86183108624BST2 promotes growth and induces gefitinib resistance in oral squamous cell carcinoma via regulating the EGFR pathwayHuang Jin0Lianping Zhang1Shufang Wang2Lei Qian3Department of Stomatology, Shanghai Songjiang District Central Hospital, Shanghai, ChinaDepartment of Stomatology, Shanghai Songjiang District Central Hospital, Shanghai, ChinaDepartment of Stomatology, Shanghai Songjiang District Central Hospital, Shanghai, ChinaDepartment of Stomatology, Shanghai Songjiang District Central Hospital, Shanghai, ChinaIntroduction 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.https://www.archivesofmedicalscience.com/BST2-promotes-growth-and-induces-gefitinib-resistance-in-oral-squamous-cell-carcinoma,108624,0,2.htmlbone marrow stromal cell antigen 2egfrgefitinib resistanceoral squamous cell carcinoma |
| spellingShingle | Huang Jin Lianping Zhang Shufang Wang Lei Qian BST2 promotes growth and induces gefitinib resistance in oral squamous cell carcinoma via regulating the EGFR pathway Archives of Medical Science bone marrow stromal cell antigen 2 egfr gefitinib resistance oral squamous cell carcinoma |
| title | BST2 promotes growth and induces gefitinib resistance in oral squamous cell carcinoma via regulating the EGFR pathway |
| title_full | BST2 promotes growth and induces gefitinib resistance in oral squamous cell carcinoma via regulating the EGFR pathway |
| title_fullStr | BST2 promotes growth and induces gefitinib resistance in oral squamous cell carcinoma via regulating the EGFR pathway |
| title_full_unstemmed | BST2 promotes growth and induces gefitinib resistance in oral squamous cell carcinoma via regulating the EGFR pathway |
| title_short | BST2 promotes growth and induces gefitinib resistance in oral squamous cell carcinoma via regulating the EGFR pathway |
| title_sort | bst2 promotes growth and induces gefitinib resistance in oral squamous cell carcinoma via regulating the egfr pathway |
| topic | bone marrow stromal cell antigen 2 egfr gefitinib resistance oral squamous cell carcinoma |
| url | https://www.archivesofmedicalscience.com/BST2-promotes-growth-and-induces-gefitinib-resistance-in-oral-squamous-cell-carcinoma,108624,0,2.html |
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