Long Noncoding RNA SNHG5 Induces the NF-KB Pathway by Regulating miR-181c-5p/CBX4 Axis to Promote the Progression of Non-Small Cell Lung Cancer
Arch. bronconeumol. (Ed. impr.)
; 59(1): 10-18, ene. 2023. ilus, graf
Article
en En
| IBECS
| ID: ibc-214117
Biblioteca responsable:
ES1.1
Ubicación: ES15.1 - BNCS
ABSTRACT
Objective: Explorations have been progressing in decoding the mechanism of non-small cell lung cancer (NSCLC). However, long noncoding RNA small nucleolar RNA host gene 5/microRNA-181c-5p/chromobox protein 4 (SNHG5/miR-181c-5p/CBX4) axis-oriented mechanisms in NSCLC is still in infancy. Therein, this study is proposed to probe this axis in NSCLC progression. Methods: Samples of 86 NSCLC patients were collected and SNHG5, miR-181c-5p and CBX4 expression was detected in NSCLC tissues and cells. NSCLC cells were transfected with plasmids to change SNHG5, miR-181c-5p or CBX4 expression, after which cell functions and phosphorylated (p)-nuclear factor (NF)-κB protein expression were evaluated. The relationships among SNHG5, miR-181c-5p and CBX4 were validated. Tumor xenografts were implemented to verify the roles of SNHG5, miR-181c-5p and CBX4 in tumor growth. Results: Low miR-181c-5p and high SNHG5 and CBX4 levels were found in NSCLC tissues and cells. Restoration of miR-181c-5p or knockdown of SNHG5 or CBX4 restrained NSCLC cell progression and inactivated the NF-κB pathway. Upregulated CBX4 abolished the effects of miR-181c-5p on reducing NSCLC cell progression. SNHG5 regulated the interaction between miR-181c-5p and CBX4. In vivo, restoration of miR-181c-5p or knockdown of SNHG5 or CBX4 retarded the tumor growth. Conclusion: This study has delineated that SNHG5 induces the NF-κB pathway by regulating the miR-181c-5p/CBX4 axis to promote NSCLC progression, which may pave a novel path for NSCLC treatment. (AU)
Palabras clave
Texto completo:
1
Colección:
06-national
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ES
Base de datos:
IBECS
Asunto principal:
Carcinoma de Pulmón de Células no Pequeñas
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MicroARNs
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Proteínas del Grupo Polycomb
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ARN Largo no Codificante
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Neoplasias Pulmonares
Límite:
Aged
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Female
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Humans
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Male
Idioma:
En
Revista:
Arch. bronconeumol. (Ed. impr.)
Año:
2023
Tipo del documento:
Article