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Identifying ATP-Binding Cassette Member B5 as a New Biomarker for Oral Squamous Cell Carcinoma
1 Oral & Maxillofacial Reconstruction, Regeneration of Luzhou Key Laboratory, Luzhou, 646000, China
2 Department of Periodontics & Oral Mucosal Diseases, The Affiliated Stomatology Hospital of Southwest Medical University, Luzhou, 646000, China
3 NHC Key Laboratory of Nuclear Technology Medical Transformation, Mianyang Central Hospital, Mianyang, 621000, China
4 Department of Pediatric Dentistry, The Affiliated Stomatology Hospital of Southwest Medical University, Luzhou, 646000, China
5 Department of Pathology, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China
6 Department of Urology, Mianyang Central Hospital, School of Medicine, University of Electronic Science and Technology of China, Mianyang, 621000, China
7 Department of Preventive Health Care, The Affiliated Stomatology Hospital of Southwest Medical University, Luzhou, 646000, China
* Corresponding Authors: Decai Wang. Email: ; Yongxian Lai. Email:
(This article belongs to the Special Issue: Novel Biomarkers and Treatment Strategies in Solid Tumor Diagnosis, Progression, and Prognosis)
Oncology Research 2025, 33(8), 2037-2053. https://doi.org/10.32604/or.2025.064276
Received 10 February 2025; Accepted 25 April 2025; Issue published 18 July 2025
Abstract
Background: Oral squamous cell carcinoma (OSCC) is the most common head and neck malignancy with a low five-year survival rate. ATP-binding cassette subfamily B member 5 (ABCB5) has been linked to tumorigenesis. However, its role in inducing OSCC remains unclear. Methods: Quantitative reverse transcription polymerase chain reaction (qRT-PCR), western blot, and immunocytochemistry (ICC) were performed to examine the level of ABCB5 in OSCC (CAL27 and HSC-3) and human oral keratinocyte (HOK). ABCB5 was knocked down in CAL27 cells using ABCB5-specific small interfering RNA (ABCB5 siRNA), and its contribution to migration, invasion, and epithelial-mesenchymal transition (EMT), a process by which epithelial cells lose their tight junction and acquire an increased migratory and invasive phenotype resembling that of mesenchymal cells, were evaluated by three-dimension and transwell migration and invasion assays, qRT-PCR and ICC. An in vivo OSCC model was established using 4-nitroquinoline-1-oxide (4NQO), a carcinogenic chemical that is commonly used to develop OSCC by destroying DNA synthesis and oxidative stress. Pathological alterations, ABCB5, and EMT markers were evaluated by H&E staining, immunohistochemistry, and qRT-PCR. Results: ABCB5 was significantly upregulated in CAL27 and HSC-3 cells as compared to HOK. Knockdown of ABCB5 significantly reduced the number of migrated and invaded CAL27 cells, accompanied by the significantly increased E-cadherin and decreased Vimentin and N-cadherin under Transforming growth factor β (TGF-β) treatment. In vivo, as OSCC advanced, a notable rise in the expressions of ABCB5, N-cadherin, and Vimentin, while a statistical decrease in E-cadherin was demonstrated. Conclusion: ABCB5 promotes the migration, invasion, and EMT of OSCC. ABCB5 might be a new biomarker and potential therapeutic target for OSCC.Keywords
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Copyright © 2025 The Author(s). Published by Tech Science Press.This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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