Osteosarcoma is a prevalent primary malignant tumor and long non-coding RNAs (lncRNAs) have been validated to modulate the osteosarcoma tumorigenesis. In present study, our research team investigates the role of a novel identified lncRNA DICER1-AS1 on the tumor progression and autophagy. Results showed that lncRNA DICER1-AS1 was up-regulated in osteosarcoma cells using microarray analysis and RT-PCR. Cellular functional experiments revealed that DICER1-AS1 knockdown suppressed the proliferation, migration, invasion and autophagy of osteosarcoma cells in vitro. Besides, DICER1-AS1 knockdown inhibited the protein expression levels of ATG5, LC3-II and Beclin 1, suggesting the inhibition on the autophagy of osteosarcoma cells. Moreover, miR-30b was verified to target 3'-UTR of DICER1-AS1 and ATG5 using bioinformatics tools and luciferase reporter assay or RNA-immunoprecipitation (RIP). Western blot showed that ATG5 protein expression was decreased in DICER1-AS1 knockdown and miR-30b mimics transfected cells, while increased in miR-30b inhibitor transfected cells, presenting a negative correlation with miR-30b and a positive correlation with DICER1-AS1. Finally, xenograft assay in vivo indicated that DICER1-AS1 knockdown inhibited the osteosarcoma tumor growth and protein expression level of ATG5. In summary, all the results conclude that DICER1-AS1 regulates the proliferation, invasion and autophagy of osteosarcoma via miR-30b/ATG5 axis, providing a novel insight for osteosarcoma tumorigenesis.
Keywords: ATG5; Autophagy; DICER1-AS1; Osteosarcoma; miR-30b.
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