Long noncoding RNA RHPN1-AS1 exerts pro-oncogenic actions in osteosarcoma by functioning as a molecular sponge of miR-506 to positively regulate SNAI2 expression.

The long noncoding RNA, RHPN1 antisense RNA 1 (), performs important regulatory actions in the progression of many human cancers. In this study, we aimed to analyze expression in osteosarcoma (OS) and to assess the influence of knockdown on the malignant behavior of OS cells. The molecular mechanisms by which affects the oncogenicity of OS were explored too. The expression of in OS was measured by RT-qPCR. The effects of the silencing in OS cells were studied both in vitro (in a Cell Counting Kit-8 assay, apoptosis analysis, and Transwell migration and invasion assays) and in vivo (by means of tumor xenografts in nude mice). Herein, expression was found to be significantly upregulated in OS tissues and cell lines. The elevated expression of closely correlated with the tumor size, TNM stage, distal metastasis and shorter overall survival in patients with OS. The depletion of restrained OS cell proliferation, migration, and invasion, and exerted proapoptotic effects in vitro. Furthermore, the knockdown of effectively reduced the tumor growth of OS cells in vivo. As for the mechanism, increased snail family zinc finger 2 (SNAI2 also known as SNAIL2) expression by acting as a competing endogenous RNA of miR-506. Notably, increasing the amount of miR-506 partially reversed the effects of the downregulation on OS cells. In conclusion, contributes to the malignancy of OS cells in vitro and in vivo, largely via upregulation of the miR-506-SNAI2 axis output.