Osteosarcoma is a common primary malignant bone tumor that occurs mainly in children and adolescents. Recent evidence has demonstrated that miR-34a is involved in the invasion and metastasis of osteosarcoma. This study aims to explore the effect of biological behavior of miR-34a on osteosarcoma. First, we collect osteosarcoma and adjacent specimens, and the relative expression of miR-34a and C-IAP2 messenger RNA was quantitated by real-time polymerase chain reaction. Furthermore, miR-34a stimulant is synthesized and transfected onto osteosarcoma MG-63 cells. The effect of overexpression of miR-34a on osteosarcoma was detected by colony-forming assay, Annexin V-fluorescein isothiocyanate Apoptosis Detection Kit I, Transwell assay, and animal experiment in vivo. Finally, the relative levels of C-IAP2 and Bcl-2 protein were checked by western blot, and the activity of caspase-3 and caspase-9 was tested by spectrophotometry assay. In conclusion, miR-34a was downregulated in osteosarcoma cells. And the expression of C-IAP2 and Bcl-2 protein was drastically inhibited, and the activities of caspase-3 and caspase-9 were significantly increased after transfecting miR-34a onto osteosarcoma MG-63 cells. And the overexpression of miR-34a can inhibit cell invasion and metastasis, promote cell apoptosis, and arrest cells in G0/G1 period. And the animal experiment in vivo demonstrated that the overexpression of miR-34a could significantly inhibit the growth of osteosarcoma in animal skin. Taken together, we indicated that miR-34a can inhibit tumor invasion and metastasis in osteosarcoma, and its mechanism may be partly related to downregulating the expression of C-IAP2 and Bcl-2 protein directly or indirectly.

Recently, lncRNAs are associated with the progression and development of various cancers. We aimed to explore the effects of lncRNA SNHG1 on the proliferation, apoptosis, migration, and invasion of oral squamous cell carcinoma (OSCC) cells. Quantitative real-time PCR (RT-qPCR) was used for measurement of SNHG1 in OSCC cells. Cell proliferation, apoptosis, migration, and invasion were detected by CCK-8 assay, flow cytometry, Cell Death Detection ELISA PLUS kit, and transwell assays. Dual-luciferase reporter assay and RNA-binding protein immunoprecipitation (RIP) assay were used to clarify the relationship between SNHG1 and miR-186. SNHG1 was overexpressed in OSCC cells. SNHG1 silencing prevented cell proliferation and increased the incidence of apoptosis, DNA fragments, cleaved-caspase 3, and Bax protein levels. Cell migration and invasion were reduced after SNHG1 deletion, and MMP2 and MMP9 protein levels were decreased. SNHG1 overexpression promoted cell survival, migration, and invasion, reduced DNA fragments formation.Mechanistically, we demonstrated that SNHG1 could directly bind to miR-186 and positively regulated α1, 6-fucosyltransferase (FUT8) level. Functional investigation showed that miR-186 depletion reversed the roles of SNHG1 silencing in cell proliferation, apoptosis, and migration. Taken together, our findings illuminated that SNHG1 regulated cell proliferation, migration, and invasion by sponging miR-186 to depress FUT8 expression.