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Long non-coding RNA CCAT1 enhances human non-small cell lung cancer growth through downregulation of microRNA-218

Long non-coding RNAs (lncRNAs) have critical functions in non-small cell lung cancer (NSCLC) growth. In the present study, we showed that lncRNA-CCAT1 was upregulated in NSCLC tissues. High expression of lncRNA-CCAT1 was related to tumor growth and reduced survival rate. We used short hairpin RNAs (...

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Detalles Bibliográficos
Autores principales: Zhao, Lijiang, Wang, Limin, Wang, Yongfeng, Ma, Ping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7057767/
https://www.ncbi.nlm.nih.gov/pubmed/32323859
http://dx.doi.org/10.3892/or.2020.7500
Descripción
Sumario:Long non-coding RNAs (lncRNAs) have critical functions in non-small cell lung cancer (NSCLC) growth. In the present study, we showed that lncRNA-CCAT1 was upregulated in NSCLC tissues. High expression of lncRNA-CCAT1 was related to tumor growth and reduced survival rate. We used short hairpin RNAs (shRNAs) to inhibit the expression of lncRNA-CCAT1 in NSCLC cells. In vitro and in vivo results demonstrated that lncRNA-CCAT1 knockdown suppressed tumor proliferation and induced apoptosis. Furthermore, microRNA-218 (miR-218) was confirmed as an effective target of lncRNA-CCAT1 in NSCLC. B lymphoma Mo-MLV insertion region 1 homolog (BMI-1), which served as a downstream target of miR-218, was also inhibited by lncRNA-CCAT1 knockdown. In conclusion, the present study indicated that upregulation of lncRNA-CCAT1 in NSCLC is associated with tumor malignant potential. lncRNA-CCAT1 enhances tumor growth in NSCLC by directly inhibiting miR-218 and indirectly increasing BMI-1 expression.