Circ_0014130 Participates in the Proliferation and Apoptosis of Nonsmall Cell Lung Cancer Cells via miR-142-5p/IGF-1 Axis

Circ_0014130 Participates in the Proliferation and Apoptosis of Nonsmall Cell Lung Cancer Cells via miR-142-5p/IGF-1 Axis: Cancer Biotherapy and Radiopharmaceuticals, Ahead of Print.



Abstract

Background: Abnormal expression of circular RNA (circRNA) has been shown to play an important role in the progression of cancer. However, the role of circRNAs on nonsmall cell lung cancer (NSCLC) remains largely unknown. This study aims to reveal the effects and potential mechanisms of circRNA on NSCLC cell proliferation and apoptosis.



Materials and Methods: Real-time quantitative polymerase chain reaction was used to detect the expression of circ_0014130 in NSCLC tissues and cells. After silencing circ_0014130 in NSCLC cells H1299 and A549, MTT assay or flow cytometry was performed to analyze the proliferation or the apoptosis of cells, respectively. The relationships between circ_0014130, miR-142-5p, and insulin-like growth factor (IGF)-1 were validated by dual-luciferase reporter system and RNA pull-down. Western blot was used to detect the protein level of IGF-1 after the interference with circ_0014130 in NSCLC cells.



Results: Circ_0014130 was abnormally highly expressed in NSCLC tissues and cells. After shRNA interfering circ_0014130 of NSCLC cells H1299 and A549, the NSCLC cell proliferation was inhibited and the cell apoptosis was promoted. By dual-luciferase reporter system and RNA pull-down assays, circ_0014130, miR-142-5p, and IGF-1 were confirmed to interact directly. After the transfection with si-circ_0014130 in NSCLC cells, the protein level of IGF-1 was reduced, and the cell proliferation was inhibited and the cell apoptosis was promoted, whereas these effects were reversed after cotransfection with miR-142-5p inhibitor.



Conclusion: Our results indicated that the silencing circ_0014130 inhibited NSCLC cell proliferation and promoted cell apoptosis by upregulating miR-142-5p and downregulating IGF-1 expression. This might provide new strategies for future diagnosis and treatment of NSCLC.