Abstract
LncRNAs have been suggested to participate in the growth and metastasis of cancer through a variety of molecular mechanisms. Recently, SNHG10, a newly discovered lncRNA, is reported to play a role of an oncogene in osteosarcoma (OS) genesis. Nonetheless, the mechanism underlying OS remains unclear. The present work found that SNHG10 expression increased within OS cells and tissues, while suppressing its expression decreased OS cell proliferation, migration, invasion, but increased their apoptosis. As for the mechanism, we confirmed that SNHG10 could bind to miR-141-3p, while the latter could bind to WTAP. SNHG10 upregulated WTAP through decreasing miR-141-3p expression. More importantly, SNHG10 deletion remarkably reduced proliferation, migration, and invasion of cells, but accelerated their apoptosis. However, when cells were subjected to miR-141-3p inhibitor cotransfection or overexpressed WTAP, these effects were partially recovered. In summary, this study suggested that the expression of SNHG10 markedly elevated within OS, and the SNHG10/miR-141-3p/WTAP axis facilitated OS progression.
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