Circular RNA circ_0046264 Suppresses Osteosarcoma Progression via microRNA-940/Secreted Frizzled Related Protein 1 Axis.

Circular RNAs (circRNAs) feature prominently in regulating tumor progression. The study aims to investigate the role and mechanism of circ_0046264 in osteosarcoma. In this study, dysregulated circRNAs in osteosarcoma tissues and adjacent tissues were screened out by analyzing circRNA microarray (GSE140256). The expressions of circ_0046264 in 58 osteosarcoma tissues and 4 osteosarcoma cell lines were detected by quantitative real-time polymerase chain reaction. Subsequently, the relationship of circ_0046264 expression level and clinical features were analyzed. Ethyldeoxyuridine assay and Transwell assay were employed to detect cell viability, migration and invasion. Dual-luciferase reporter assay was adopted to confirm the targeting relationships between circ_0046264 and microRNA-940 (miR-940), as well as miR-940 and secreted frizzled related protein 1 (SFRP1). SFRP1 expression was determined by western blot. Here, we demonstrated that circ_0046264 was greatly down-regulated in osteosarcoma and was inversely related to tumor size and Ki67 expression. Functional assays validated that circ_0046264 could restrain the proliferation, migration and invasion. Mechanistically, circ_0046264 could adsorb miR-940 and indirectly modulate SFRP1 expression. Furthermore, the transfection of miR-940 mimics or SFRP1 small interfering RNA could reverse the impact of circ_0046264 overexpression on the growth, migration and invasion of osteosarcoma cells. Taken together, circ_0046264 is a tumor suppressor to inhibit the osteosarcoma progression via modulating the miR-940 / SFRP1 axis.

Long noncoding RNA LINC00341 promotes the vascular smooth muscle cells proliferation and migration via miR-214/FOXO4 feedback loop.

Increasing evidences have indicated the vital roles of long noncoding RNA (lncRNA) in the atherosclerosis. However, whether lncRNA LINC00341 play pivotal roles in the vascular smooth muscle cells (VSMCs) is still unclear. This work presents the authentic functions of LINC00341 on the proliferation and migration of VSMCs and unveils the underlying mechanism. Functional experiment data demonstrated that LINC00341 expression was increased in the ox-LDL induced VSMCs with dose-dependent and time-dependent mode. Moreover, the knockdown of LINC00341 suppressed the proliferation and migration ability of VSMCs. Mechanically, we found that LINC00341 promoted the FOXO4 protein expression via sponging miR-214, which, in return, resulting in the transcription activation of LINC00341. In conclusion, the results conclude that LINC00341 promotes the proliferation and migration of VSMCs and confirm the positive feedback loop of LINC00341/miR-214/FOXO4 axis.