Long noncoding RNA LINC01410 promotes tumorigenesis of osteosarcoma cells via miR-497-5p/HMGA2 axis

LINC01410 is a tumor promoter that is upregulated in some cancer types, such as osteosarcoma (OS). Nonetheless, its role in OS and the underlying molecular mechanism have not been fully understood. Hence, we sought to elucidate it. We performed reverse-transcription quantitative polymerase chain reaction for examining LINC01410, miR-497-5p and HMGA2 levels. Additionally, we carried out the cell counting kit-8 and Transwell assays for detecting cell proliferation and invasion/migration. Bioinformatics predicted that there was a miR-497-5p binding site in LINC01410 or HMGA2; meanwhile, miR-497-5p was found to interact with HMGA2 and LINC01410 through dual-luciferase reporter assay. LINC01410 and HMGA2 were high, and miR-497-5p showed low expression in OS tissues and cells. Cell function assay demonstrated that LINC01410 or HMGA2 knockdown or miR-497-5p overexpression obviously restrained OS proliferation, invasion, and migration. Oppositely, inhibiting miR-497-5p had the opposite effects. Functionally, miR-497-5p bound with LINC01410 3 '-untranslated region and HMGA2 was found to be the miR-497-5p target gene. Lastly, LINC01410 enhanced OS cell growth, invasion, and migration via decreasing miR-497-5p expression, whereas increasing that of HMGA2. We have demonstrated that LINC01410 promoted OS development partly by miR-497-5p/HMGA2 signal transduction pathway and this provides a reference for studying the mechanism of LINC01410 in OS.

Automated summary

LINC01410 has been identified as a tumor promoter in osteosarcoma, with its mechanism partially involving the miR-497-5p/HMGA2 signaling pathway. This finding provides a valuable reference for further studies on the role of LINC01410 in osteosarcoma.