circHIPK3 Acts as Competing Endogenous RNA and Promotes Non-Small-Cell Lung Cancer Progression through the miR-107/BDNF Signaling Pathway

• Published in: BioMed research international 2020, Vol.2020 (2020), p.1-9
• Main Authors: Xie, Haixiang, Yang, Qilian, Ding, Jingyi, Zhang, Yajuan, Hong, Weijun, Gao, Xiwen
• Format: Article
• Language: English
• Subjects: 3' Untranslated regions; Assaying; Base Sequence; Bioinformatics; Biomedical research; Brain-derived neurotrophic factor; Brain-Derived Neurotrophic Factor - metabolism; Carcinoma, Non-Small-Cell Lung - genetics; Carcinoma, Non-Small-Cell Lung - pathology; Cell adhesion & migration; Cell cycle; Cell growth; Cell Line, Tumor; Cell proliferation; Cell Proliferation - genetics; Down-Regulation - genetics; Gene expression; Gene Expression Regulation, Neoplastic; Gene Knockdown Techniques; Humans; Lung cancer; Lung Neoplasms - genetics; Lung Neoplasms - pathology; Medical treatment; Metabolism; Metastasis; MicroRNAs; MicroRNAs - genetics; MicroRNAs - metabolism; Neoplasm Invasiveness; Non-small cell lung carcinoma; Plasmids; Regulatory mechanisms (biology); Ribonucleic acid; RNA; RNA, Circular - genetics; RNA, Circular - metabolism; Signal Transduction; Small cell lung carcinoma; Transfection; Tumorigenesis
• ISSN: 2314-6133; 2314-6141
• DOI: 10.1155/2020/6075902

Circular RNAs (circRNAs) act as a crucial part in many human diseases, particularly in cancers. circRNA HIPK3 (circHIPK3) is a special circRNA that may participate in the oncogenesis of non-small-cell lung cancer (NSCLC), even though its latent regulatory mechanism is not very clear. Here, we studied the roles of circHIPK3 in NSCLC. qRT-PCR assay was applied to study the expression of circHIPK3 in NSCLC. The influence of circHIPK3 on NSCLC was estimated by silencing circHIPK3 and miR-107 mock transfection and brain-derived neurotrophic factor (BDNF) overexpression, and the correlation between circHIPK3, miR-107, and BDNF was evaluated by dual-luciferase reporter assay. The results showed that circHIPK3 expression was upregulated in NSCLC cells. circHIPK3 knockdown inhibited the migration and proliferation of NSCLC cells by promoting the expression of miR-107. circHIPK3 could be used as a miR-107 sponge to promote BDNF cell proliferation. The dual-luciferase reporter assay proved that miR-107 was the target of circHIPK3, and miR-107 had an interaction with the 3′untranslated region of BDNF. miR-107 overexpression inhibited BDNF-mediated NSCLC cell proliferation. These results indicate that circHIPK3 promotes tumor progression through a new circHIPK3/miR-107/BDNF axis, which offers potential markers and medical treatment for NSCLC.