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SOX18 meditates the resistance of Bmi1‐expressing cells to cetuximab in HNSCC.
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- Author(s): Zhang, Caihua; Chen, Zhi; Gao, Nailin; Xiong, Gan; Chen, Peng; Li, Hui; Chen, Demeng; He, Qianting; Peng, Liang
- Source:
Oral Diseases; Apr2024, Vol. 30 Issue 3, p1100-1113, 14p- Subject Terms:
SQUAMOUS cell carcinoma; PROTEINS; BIOLOGICAL models; PHOSPHORYLATION; RESEARCH funding; HEAD & neck cancer; ANTINEOPLASTIC agents; TRANSCRIPTION factors; TREATMENT effectiveness; FLUORESCENT antibody technique; REVERSE transcriptase polymerase chain reaction; DESCRIPTIVE statistics; CELLULAR signal transduction; MONOCLONAL antibodies; MICE; IMMUNOHISTOCHEMISTRY; RNA; GENE expression; ENERGY metabolism; CELL lines; ANIMAL experimentation; WESTERN immunoblotting; GENE expression profiling; STEM cells; COMPARATIVE studies; SEQUENCE analysis; EVALUATION; PHARMACODYNAMICS - Source:
- Additional Information
- Abstract: Objective: Head and neck squamous cell carcinoma (HNSCC) is the most common type of malignancy in the head and neck region worldwide. The therapeutic strategies for HNSCC remain unsatisfying and limited. Here, we found a population of resistant Bmi1‐expressing cells in the presence of cetuximab treatment and reported a novel role of SRY‐box transcription factor 18 (SOX18), a member of the SOX family, in promoting HNSCC resistance to cetuximab. This study aimed to investigate the regulatory mechanism of Sox18 in Bmi1‐positive cells and to search for better therapeutic targets. Methods: We successfully obtained Bmi1CreER, RosatdTomato, and RosaDTA mice and identified Bmi1‐expressing cells through lineage tracing. SOX18 expression in HNSCC and normal tissues was analyzed by immunohistochemistry, colocalization of Sox18, and Bmi1‐expressing cells was analyzed by immunofluorescence, and SOX18 expression in SCC9 cell lines was quantified by western blotting and quantitative real‐time PCR. The investigation of the mechanism of SOX18‐mediated cetuximab resistance in Bmi1‐positive cells was based on the analysis of single‐cell RNA‐seq data obtained from the Gene Expression Omnibus (GEO) database. Western blotting was performed to verify the results obtained from the single‐cell RNA‐seq analysis. Results: In our study, we demonstrated that Bmi1‐expressing cells were resistant to cetuximab treatment and that depletion of Bmi1‐expressing cells improved cetuximab efficacy in HNSCC. We then discovered that Sox18 mediated the stem cell‐like properties of Bmi1‐expressing cells and promoted cellular cetuximab resistance through an oxidative phosphorylation pathway. There was a significant downregulation of key genes in the oxidative phosphorylation pathway in Sox18 knockout cell lines. Conclusions: Taken together, the findings of our study suggest that Sox18 mediates the resistance of Bmi1‐expressing cells to cetuximab in HNSCC via the oxidative phosphorylation pathway. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Oral Diseases is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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