Long Noncoding RNA SNHG5 Induces the NF-κB Pathway by Regulating miR-181c-5p/CBX4 Axis to Promote the Progression of Non-Small Cell Lung Cancer

Shiyang Kang; Chaopeng Ou; An Yan; Kaibin Zhu; Ruifeng Xue; Yingjun Zhang; Jielan Lai

Ayuda

Long Noncoding RNA SNHG5 Induces the NF-κB Pathway by Regulating miR-181c-5p/CBX4 Axis to Promote the Progression of Non-Small Cell Lung Cancer

Shiyang Kang ^[1] ; Chaopeng Ou ^[1] ; An Yan ^[2] ; Kaibin Zhu ^[2] ; Ruifeng Xue ^[1] ; Yingjun Zhang ^[1] ; Jielan Lai ^[1]
1. [1] Sun Yat-sen University Cancer Center
  
  Sun Yat-sen University Cancer Center
  
  China
2. [2] Harbin Medical University
  
  Harbin Medical University
  
  China
Localización: Archivos de bronconeumología: Organo oficial de la Sociedad Española de Neumología y Cirugía Torácica SEPAR y la Asociación Latinoamericana de Tórax ( ALAT ), ISSN 0300-2896, Vol. 59, Nº. 1 (January), 2023, págs. 10-18
Idioma: inglés
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Resumen
- 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.