# Identifying ATP-Binding Cassette Member B5 as a New Biomarker for Oral Squamous Cell Carcinoma

## TL;DR

This study shows that ABCB5 promotes cancer spread in oral squamous cell carcinoma and could be a new target for treatment.

## Contribution

ABCB5 is identified as a novel biomarker and potential therapeutic target for oral squamous cell carcinoma.

## Key findings

- ABCB5 was significantly upregulated in OSCC cell lines compared to normal cells.
- ABCB5 knockdown reduced cancer cell migration and invasion and altered EMT markers.
- In vivo, ABCB5 expression increased with OSCC progression and was linked to EMT markers.

## Abstract

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.

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.

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.

ABCB5 promotes the migration, invasion, and EMT of OSCC. ABCB5 might be a new biomarker and potential therapeutic target for OSCC.