circCCND1 Regulates Oxidative Stress and FGF9 to Enhance Chemoresistance of Non-Small Cell Lung Cancer via Sponging miR-187-3p

Abstract

Circular RNAs have been shown to regulate cancer tumorigenesis and drug resistance. Recently, circCCND1 is reported to promote laryngeal squamous cell carcinoma; however, whether circCCND1 is implicated in non-small cell lung cancer (NSCLC) remains unclear. In this research, The Cancer Genome Atlas data of lung adenocarcinoma were analyzed to show gene expression and overall survival. 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di- phenytetrazoliumromide assay and cell colony formation assay were utilized to measure cell viability and proliferation of A549 and HCC827. Apoptosis was detected by TdT-mediated dUTP Nick-End Labeling assay. Besides, reverse transcription-quantitative PCR was used to examine gene expression. We observed that circCCND1 was significantly upregulated in lung cancer cells and patients. circCCND1 knockdown attenuated cell proliferation and induced apoptosis under cisplatin treatment. Mechanistically, circCCND1 interacted with miR-187-3p to regulate reactive oxygen species and FGF9 in NSCLC cells. Finally, miR-187-3p was demonstrated to rescue circCCND1 knockdown-modulated chemoresistance of NSCLC cells. In this study, our conclusions facilitate the understanding of NSCLC drug resistance to cisplatin.