Circular RNA circ_001621 acts as a tumor promoter in lung cancer by regulating the miR-199a-3p/GREM1 axis.
Arch Med Sci
; 20(3): 876-886, 2024.
Article
em En
| MEDLINE
| ID: mdl-39050152
ABSTRACT
Introduction:
Investigating how circular RNAs (circRNAs) function during tumorigenesis may help uncover novel diagnostic markers for cancer treatment. The oncogenic role of circ_001621 has been verified in osteosarcoma, but its role in lung cancer has yet to be reported. This research is the first to investigate the circ_001621 expression and regulatory mechanism in lung cancer. Material andmethods:
RT-qPCR was performed to assess the circ_001621 expression levels in lung cancer cells and tissues. The influence of circ_001621 on the viability, invasive ability, and apoptosis of lung cancer cells was investigated through CCK-8, transwell, and caspase-3 activity experiments, respectively. A xenograft nude mouse model was designed to evaluate how circ_001621 functions in vivo. The RIP and luciferase reporter experiments confirmed the binding among circRNA, miRNA, and mRNA.Results:
Circ_001621 was dramatically upregulated in lung cancer tissues and cells. Silencing circ_001621 in lung cancer cells reduced their viability and invasive ability but stimulated apoptosis. The nude mice experiment demonstrated that circ_001621 downregulation considerably stunted tumor growth in vivo. Additionally, circ_001621 could sponge miR-199a-3p. The inhibitor of miR-199a-3p improved the viability and invasion of cells while inhibiting apoptosis. Moreover, it offset the impact of circ_001621 on lung cancer cells. MiR-199a-3p was observed to target GREM1, and the downregulation of GREM1 could counteract miR-199a-3p-induced effects on lung cancer cells.Conclusions:
The circ_001621/miR-199a-3p/GREM1 axis exhibits an association with the development of lung cancer, suggesting its potential as a future therapeutic target for the disease.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Idioma:
En
Ano de publicação:
2024
Tipo de documento:
Article