lncRNA RPSAP52 induced the development of tongue squamous cell carcinomas via miR-423-5p/MYBL2.
J Cell Mol Med
; 25(10): 4744-4752, 2021 05.
Article
em En
| MEDLINE
| ID: mdl-33787061
ABSTRACT
Growing lncRNAs have been noted to involve in the initiation and development of several tumours including tongue squamous cell carcinomas (TSCCs). However, the biological role and mechanism of lncRNA RPSAP52 were not well-explained. We indicated that RPSAP52 was higher in TSCC samples compared with that in control samples. The higher expression of RPSAP52 was positively correlated with higher T stage and TNM stage. Ectopic expression of RPSAP52 induced TSCC cell growth and cycle and induced cytokine secretion including IFN-γ, IL-1ß and IL-6, IL-8, IL-10 and TGF-ß. We found that the overexpression of RPSAP52 suppressed miR-423-5p expression in SCC-4 cell. miR-423-5p was lower in TSCC samples compared with that in control samples, and miR-423-5p level was negatively correlated with higher T stage and TNM stage. Pearson's correlation indicated that miR-423-5p was negatively associated with that of RPSAP52 in TSCC tissues. Furthermore, MYBL2 was one direct gene of miR-423-5p and elevated expression of miR-423-5p suppressed MYBL2 expression and ectopic expression of RPSAP52 increased MYBL2 expression in SCC-4 cell. Finally, we illustrated that RPSAP52 overexpression promoted TSCC cell growth and cycle and induced cytokine secretion including IFN-γ, IL-1ß and IL-6, IL-8, IL-10 and TGF-ß via modulating MYBL2. These data provided new insight into RPSAP52, which may be one potential treatment target for TSCC.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Neoplasias da Língua
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Carcinoma de Células Escamosas
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Biomarcadores Tumorais
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Regulação Neoplásica da Expressão Gênica
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Transativadores
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Proteínas de Ciclo Celular
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MicroRNAs
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RNA Longo não Codificante
Tipo de estudo:
Observational_studies
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Prognostic_studies
/
Risk_factors_studies
Limite:
Humans
Idioma:
En
Ano de publicação:
2021
Tipo de documento:
Article