MALAT1 induces osteosarcoma progression by targeting miR‐206/CDK9 axis.

Long noncoding RNAs (LncRNAs) have been reported to participate in cancer development, including osteosarcoma. Here, in our study, we observed that lncRNA metastasis‐associated lung adenocarcinoma transcription 1 (MALAT1) was remarkably overexpressed in osteosarcoma. However, the role it plays in osteosarcoma proliferation mediated by miR‐206/cyclin‐dependent kinase 9 (CDK9) axis remains uninvestigated. It was found that miR‐206 was decreased and CDK9 was elevated in human osteosarcoma cells including MG63, Saos‐2, U2OS, and KHOS compared with human osteoblast cell line hFOB 1.19. In addition, it was exhibited that knockdown of MALAT1 was able to inhibit osteosarcoma cell proliferation, which suggested that MALAT1 played an oncogenic role in osteosarcoma development. Bioinformatics analysis indicated that MALAT1 can function as a competing endogenous RNA by sponging miR‐206. Because miR‐206 has been identified as a significant tumor suppressive gene in multiple cancers, we validated that mimics of miR‐206 can restrain osteosarcoma progression. Furthermore, dual‐luciferase reporter assay, RNA binding protein immunoprecipitation, and RNA pull‐down assay demonstrated the correlation between miR‐206 and MALAT1. Besides these, CDK9 was predicted as a downstream gene of miR‐206, and we observed that MALAT1 can regulate osteosarcoma progress by modulating CDK9 expression via sponging miR‐206. In conclusion, our study implied that MALAT1/miR‐206/CDK9 axis can provide novel insights into the biological mechanism of osteosarcoma progression. We found that metastasis‐associated lung adenocarcinoma transcription 1 (MALAT1) inhibition can repress osteosarcoma development by regulating miR‐206 and cyclin‐dependent kinase 9 (CDK9) in vitro, and a negative correlation between MALAT1 and miR‐206 was confirmed in our study. In addition, we observed that MALAT1 can regulate CDK9 expression by sponging miR‐206. Hence, it was concluded that MALAT1/miR‐206/CDK9 axis was responsible for osteosarcoma progression. [ABSTRACT FROM AUTHOR]