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Knockdown of LINC00662 represses AK4 and attenuates radioresistance of oral squamous cell carcinoma
BACKGROUND: LncRNAs play crucial roles in the development of carcinomas. However, the investigation of LINC00662 in Oral squamous cell carcinoma (OSCC) is still elusive. METHODS: qRT-PCR assay tested the expression levels of LINC00662, hnRNPC and AK4. With exposure to irradiation, CCK-8, colony form...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7296632/ https://www.ncbi.nlm.nih.gov/pubmed/32549791 http://dx.doi.org/10.1186/s12935-020-01286-9 |
Sumario: | BACKGROUND: LncRNAs play crucial roles in the development of carcinomas. However, the investigation of LINC00662 in Oral squamous cell carcinoma (OSCC) is still elusive. METHODS: qRT-PCR assay tested the expression levels of LINC00662, hnRNPC and AK4. With exposure to irradiation, CCK-8, colony formation, flow cytometry and western blot experiments, respectively determined the function of LINC00662 in the radiosensitivity of OSCC cells. Then RIP and western blot assays affirmed the interaction between hnRNPC protein and LINC00662 or AK4. Finally, rescue assays validated the regulation mechanism of LINC00662 in the radioresistance of OSCC. RESULTS: In the present report, LINC00662 was overexpressed in OSCC and its silencing could alleviate radioresistance of OSCC. Furthermore, the interaction between hnRNPC protein and LINC00662 or AK4 was uncovered. Besides, LINC00662 regulated AK4 mRNA stability through binding to hnRNPC protein. To sum up, LINC00662 modulated the radiosensitivity of OSCC cells via hnRNPC-modulated AK4. CONCLUSION: The molecular mechanism of the LINC00662/hnRNPC/AK4 axis was elucidated in OSCC, which exhibited a promising therapeutic direction for patients with OSCC. |
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