ZFAS1 Promotes Cisplatin Resistance via Suppressing miR-421 Expression in Oral Squamous Cell Carcinoma
| Autor: | Rui Hao, Fan Wang, Xiao‐Long Wang, Feng‐Juan Wang |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Cisplatin endocrine system diseases medicine.diagnostic_test Chemistry Cell growth Cell Exosome Flow cytometry stomatognathic diseases 03 medical and health sciences 030104 developmental biology 0302 clinical medicine medicine.anatomical_structure Oncology Apoptosis In vivo 030220 oncology & carcinogenesis medicine Cancer research Viability assay medicine.drug |
| Zdroj: | Cancer Management and Research. 12:7251-7262 |
| ISSN: | 1179-1322 |
| DOI: | 10.2147/cmar.s248869 |
| Popis: | Purpose Oral squamous cell carcinoma (OSCC), with high incidence and mortality, represents one of the main reasons for head and neck malignant tumors. We want to investigate the effect of ZFAS1 on DDP resistance in oral squamous cell carcinoma. Methods The proliferation and migration of cells was detected by CCK-8 and Transwell assay. The apoptosis was measured by flow cytometry and Western blot. The interaction of ZFAS1, miR-421, and MEIS2 was verified by luciferase reporter assay. The role of ZFAS1 in DDP resistance in vivo was tested by the nude mice model. The expression of ZFAS1 in exosomes from cisplatin-resistant patients was also determined. Results ZFAS1 overexpression improved OSCC cell growth and inhibited OSCC cell susceptibility to DDP. In addition, the silencing of ZFAS1 promoted DDP-induced apoptosis. ZFAS1 directly bound to miR-421, which was verified by luciferase reporter assay. Inhibition of miR-421 reversed the effect of si-ZFAS1, which promoted the cell viability and decreased the sensitivity of DDP in DDP-resistant cells. The in vivo experiment showed the role of ZFAS1 in increasing the DDP resistance in OSCC tumor. Importantly, this study also showed upregulated ZFAS1 in serum exosomes derived from cisplatin-resistant patients. Conclusion ZFAS1 promotes chemoresistance of oral squamous cell carcinoma to cisplatin and might become a latent therapeutic target for treating OSCC. |
| Databáze: | OpenAIRE |
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