Background. Osteosarcoma (OS) is one of the most malignant bone tumors and has a high metastatic rate. Increasing research has demonstrated the vital roles of long noncoding RNAs (lncRNAs) in human cancers, including OS. LncRNA LINC00662 has been revealed to act as an oncogene involved in multiple tumor progression. This study aimed to investigate the expression pattern, function, and regulatory mechanism of LINC00662 in OS. Methods. Patients who underwent OS surgery were involved in this study. Experiments including RT-qPCR, MTT, western blot, FISH, RNA pull-down, luciferase reporter, colony formation, transwell invasion and migration, and sphere formation assay were performed to investigate the regulatory role of LINC00662 in OS. Results. In the present study, our findings demonstrated the upregulation of LINC00662 expression in OS tissues and cells, and high expression of LINC00662 predicted a poor clinical prognosis of patients’ iNOS. Through a series of in vivo assays, LINC00662 knockdown suppressed OS cell proliferation, invasion, migration, and stemness property maintenance. Further mechanistical investigations indicated that LINC00662 functioned as a competing endogenous RNA (ceRNA) for sponging microRNA-16-5p (miR-16-5p) to upregulate the expression of IP receptor type 1 (ITPR1) in OS cells. Restoration assays validated the involvement of ITPR1 in LINC00662-mediated regulation of cell functions in OS. Conclusion. LINC00662 exerts oncogenic functions in OS by targeting the miR-16-5p/ITPR1 axis.
We showed that miR-107 expression was decreased in osteosarcoma (OS) tissues and cell lines. miR-107 mimic significantly decreased OS cell proliferation and inhibited invasion and migration of OS cells. Inhibition of miR-107 expression notably promoted proliferation, invasion and migration of OS cells. In addition, miR-107 mimic inhibited EMT biomarkers and significantly increased apoptosis. miR-107 mimic significantly decreased the protein expression of β-catenin, Cyclin D1, and c-Myc, whereas increased GSK-3β protein expression. miR-107 mimic markedly reduced the luciferase activity of 3'UTR of β-catenin. Overexpression of β-catenin inhibited miR-107 mimic-induced decrease of cell proliferation, invasion and migration ability, and increase of apoptosis.
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