BACKGROUND: In this work, we investigated the functional role of microRNA 137 (miR-137) in regulating osteosarcoma both in vitro and in vivo. METHODS: Quantitative RT-PCR was used to examine the gene expressions of miR-137 in osteosarcoma cell lines and osteosarcoma tumors. 143B and Saos-2 cells were infected with lentivirus expressing miR-137 mimics (miR-137-mimic) to ectopically upregulate miR-137. In vitro cancer proliferation and migration were examined by MTT assay and transwell assay, respectively. Viral infected Saos-2 cells were also subcutaneously inoculated into null mice to evaluate the effect of miR-137 upregulation on in vivo tumor growth. The interaction between miR-137 and its downstream target, FXYD6, was evaluated by dual-luciferase reporter assay and quantitative real-time PCR. FXYD6 was then subsequently upregulated in osteosarcoma cells to evaluate its effect on miR-137 regulation in osteosarcoma. RESULTS: We found that miR-137 was significantly downregulated in both osteosarcoma cell lines and osteosarcoma tumors. Lentiviral infection of miR-137-mimic upregulated miR-137 gene expression, reduced in vitro proliferation and migration and inhibited in vivo osteosarcoma tumor growth. FXYD6 was verified to be directly interacting with miR-137, and its subsequent upregulation reversed the inhibitory effect of miR-137 upregulation in osteosarcoma. CONCLUSION: We revealed novel functional role of miR-137 in osteosarcoma regulation, likely through FXYD6 binding.
BACKGROUND: In this work, we investigated the functional role of microRNA 137 (miR-137) in regulating osteosarcoma both in vitro and in vivo. METHODS: Quantitative RT-PCR was used to examine the gene expressions of miR-137 in osteosarcoma cell lines and osteosarcoma tumors. 143B and Saos-2 cells were infected with lentivirus expressing miR-137 mimics (miR-137-mimic) to ectopically upregulate miR-137. In vitro cancer proliferation and migration were examined by MTT assay and transwell assay, respectively. Viral infected Saos-2 cells were also subcutaneously inoculated into null mice to evaluate the effect of miR-137 upregulation on in vivo tumor growth. The interaction between miR-137 and its downstream target, FXYD6, was evaluated by dual-luciferase reporter assay and quantitative real-time PCR. FXYD6 was then subsequently upregulated in osteosarcoma cells to evaluate its effect on miR-137 regulation in osteosarcoma. RESULTS: We found that miR-137 was significantly downregulated in both osteosarcoma cell lines and osteosarcoma tumors. Lentiviral infection of miR-137-mimic upregulated miR-137 gene expression, reduced in vitro proliferation and migration and inhibited in vivo osteosarcoma tumor growth. FXYD6 was verified to be directly interacting with miR-137, and its subsequent upregulation reversed the inhibitory effect of miR-137 upregulation in osteosarcoma. CONCLUSION: We revealed novel functional role of miR-137 in osteosarcoma regulation, likely through FXYD6 binding.
Authors: G M Viera; K B Salomao; G R de Sousa; M Baroni; L E A Delsin; J A Pezuk; M S Brassesco Journal: Clin Transl Oncol Date: 2019-04-04 Impact factor: 3.405