Circ_0087378 intensifies the malignant behavior of non-small cell lung cancer cells in vitro by facilitating DDR1 via sponging miR-199a-5p

Abstract

Background Circular RNA hsa_circ_0087378 (circ_0087378) has been found to have different functions in different cancer types. However, its function in non-small cell lung cancer (NSCLC) remains unclear. This study revealed the effect of circ_0087378 on the malignant behavior of NSCLC cells in vitro to broaden the options for NSCLC treatment. Methods This study detected the expression of circ_0087378 in NSCLC cells via real-time quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The discoidin domain receptor 1 (DDR1) protein in NSCLC cells was investigated through western blot. The influence of circ_0087378 on the malignant behavior of NSCLC cells in vitro was investigated by cell counting kit-8 assay, colony formation assay, Transwell assay, and flow cytometry. Dual-luciferase reporter gene assay and RNA pull-down assay were performed to verify the binding between two genes. Results Circ_0087378 was abundantly expressed in NSCLC cells. The loss of circ_0087378 repressed the proliferation, colony formation, migration, invasion, but enhanced the apoptosis in NSCLC cells in vitro . Circ_0087378 could repress microRNA-199a-5p (miR-199a-5p) by acting as a sponge. The loss of miR-199a-5p abrogated the inhibition of circ_0087378 loss on the malignant phenotype of NSCLC cells in vitro . DDR1 was directly repressed via miR-199a-5p. DDR1 counteracted the repressive role of miR-199a-5p on the malignant behavior of NSCLC cells in vitro . Conclusions Circ_0087378 promotes the malignant behavior of NSCLC cells in vitro by facilitating DDR1 via sponging miR-199a-5p. It may be a promising target for treatment.

Circ_0070934 promotes MGAT3 expression and inhibits epithelial-mesenchymal transition in bronchial epithelial cells by sponging miR-199a-5p

“…Another study has shown that miR-199a-5p could regulate mesenchymal stem cell senescence in patients with idiopathic pulmonary fibrosis by regulating Sirt1/AMPK signaling pathway [ 12 ]. Previous studies have shown that certain circRNAs can bind competitively to miR-199a-5p to form miR-199a-5p response elements, thereby reducing their negative regulation of target genes, that is, influencing occurrence and development of non-small cell lung cancer through the competitive endogenous RNA (ceRNA) mechanism [ 13 , 14 ]. However, whether it is involved in the biological process of asthma through the ceRNA mechanism, affecting bronchial epithelial cells apoptosis and EMT, remains unclear.…”