hsa_circ_0009618 sponges miR-152-3p to promote lung adenocarcinoma progression

Abstract

Abstract Background Accumulating evidence suggests circular RNAs (circRNAs) act as regulators in cancer progression. However, the function of circRNAs in lung adenocarcinoma is still uncertain. The purpose of this study was to investigate the function of hsa_circ_0009618 in lung adenocarcinoma progression. Methods CircRNA microarray was performed to screen circRNA expression profiles of lung adenocarcinoma. hsa_circ_0009618 was identified for further study and verified by quantitative real-time PCR (qRT-PCR) in lung adenocarcinoma tissues and cell lines. Cell proliferation was examined by 3-(4,5-Dimethylthiazol-2-yl)- 2,5-diphenyltetrazolium bromide (MTT) and cell cycles assay, cell migration were detected by wound-healing assay and transwell assays. Tumorigenesis in nude mice was performed to assess the effect of hsa_circ_0009618 on lung adenocarcinoma. Bioinformatics analysis and luciferase reporter assay were used to demonstrate the mechanism of hsa_circ_0009618. Results Hsa_circ_0009618 was upregulated in lung adenocarcinoma tissues and cells. Functional experiments suggested that knockdown of hsa_circ_0009618 could inhibit the lung adenocarcinoma cell viability, migration and invasion.The down-regulation of hsa_circ_0009618 increased the number of cells in S phase and decreased the number of cells in G1.hsa_circ_0009618 knockdown also inhibited the volume and weight of tumors than those in the control group. In addition, we demonstrated that hsa_circ_0009618 could bind to miR-153-3p and targets Hmga2 expression to promote the progression of lung adenocarcinoma. Conclusion Our results suggested that hsa_circ_0009618 promotes the progression of lung adenocarcinoma through targeting the miR-153-3p / Hmga2 axis, and it might serve as a potential therapy target for lung adenocarcinoma.