Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0029463 (osteosarcoma)
 16,637 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this exploration was to detect the biological effects of miR-10b/FAM46C pair on osteosarcoma (OS) development. By accessing to the Gene Expression Omnibus (GEO) database, we achieved expressional profiles of miR-10b and FAM46C. Kaplan-Meier method was applied to determine the overall survival rates of OS patients. MiR-10b mimic/inhibitor were utilized to alter miR-10b expression. Overexpression of FAM46C was induced by pcDNA3.1-FAM46C. QRT-PCR and western blot were conducted to assess the expression levels. Cell counting kit-8 (CCK-8) and transwell assays were employed to evaluate the proliferative, invasive and migratory properties of OS cells. Pearson correlation analysis was performed to confirm the association between miR-10b and FAM46C. Dual-luciferase reporter assay was conducted to determine the target of miR-10b. The overall survival of OS patients was inversely correlated with miR-10b expression. MiR-10b was increased in OS compared with normal controls. Depletion of miR-10b attenuated the proliferation, invasion and migration of MG-63 cells. FAM46C was considered as a target gene of miR-10b and inversely related with miR-10b. Overexpression of FAM46C could inhibit cell growth, invasion and migration in OS; furthermore, it also can enforced the miR-10b inhibitor-induced effects on cell behaviors of OS cells. Down-regulation of miR-10b played a suppressive effect on the cell activity in OS cells, which provides a novel insight into the advance of OS therapeutic therapies.
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PMID:Down-regulation of miR-10b represses cell vitality in osteosarcoma and is inversely associated with prognosis via interacting with FAM46C: Running title: MiR-10b/FAM46C axis modulates OS progression. 3222 57