RP11156L14.1 regulates SSR1 expression by competitively binding to miR548ao3p in hypopharyngeal squamous cell carcinoma.
Oncol Rep
; 44(5): 2080-2092, 2020 11.
Article
en En
| MEDLINE
| ID: mdl-33000261
ABSTRACT
Emerging studies have demonstrated that long noncoding RNAs (lncRNAs) play essential roles in tumorigenesis. However, the role and function of lncRNAs in hypopharyngeal squamous cell carcinoma (HSCC) have not been completely elucidated. The present study explored the function of a novel lncRNA, RP11156L14.1, in HSCC. RP11156L14.1 was revealed to be highly expressed in HSCC tissues and cell lines. Knockdown of RP11156L14.1 inhibited proliferation, migration, and invasion in HSCC cells. Furthermore, RP11156L14.1 regulated epithelialmesenchymal transition (EMT) by controlling EMTrelated protein expression. Mechanistically, RP11156L14.1 exerted its function as a competing endogenous RNA (ceRNA) and directly interacted with miR548ao3p. The present study also demonstrated that miR548ao3p regulated signal sequence receptor subunit 1 (SSR1) expression by targeting SSR1 3'UTR. Moreover, the xenograft HSCC tumor model revealed that knockdown of RP11156L14.1 markedly suppressed HSCC tumor growth in vivo. In summary, these findings indicated that the lncRNA RP11156L14.1 functions as an oncogene in HSCC by competing with miR548ao3p in regulating SSR1 expression. The RP11156L14.1/miR548ao3p/SSR1 axis could be utilized as a potential novel biomarker and therapeutic target for HSCC.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Proteínas de Unión al Calcio
/
Glicoproteínas de Membrana
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Neoplasias Hipofaríngeas
/
Receptores de Péptidos
/
Receptores Citoplasmáticos y Nucleares
/
MicroARNs
/
ARN Largo no Codificante
/
Carcinoma de Células Escamosas de Cabeza y Cuello
Tipo de estudio:
Observational_studies
/
Prognostic_studies
Límite:
Adult
/
Aged
/
Animals
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Female
/
Humans
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Male
/
Middle aged
Idioma:
En
Revista:
Oncol Rep
Asunto de la revista:
NEOPLASIAS
Año:
2020
Tipo del documento:
Article