ArticleOncoTargets and therapy2015
miR-205 suppresses the proliferative and migratory capacity of human osteosarcoma Mg-63 cells by targeting VEGFA.
Article in OncoTargets and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Long non-coding RNA NEAT1 promotes colorectal cancer progression by regulating miR-205-5p/VEGFA axis.Human cell · 2020Article
- Anti-tumoral potential of MDA19 in human osteosarcoma via suppressing PI3K/Akt/mTOR signaling pathway.Bioscience reports · 2018Article
- Identification of Novel Target for Osteosarcoma by Network Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- MicroRNA-205 is downregulated in hepatocellular carcinoma and inhibits cell growth and metastasis via directly targeting vascular endothelial growth factor A.Oncology letters · 2018Article
- miR-205 Inhibits Neuroblastoma Growth by Targeting cAMP-Responsive Element-Binding Protein 1.Oncology research · 2018Article
- Long noncoding RNA MALAT1 promotes cell proliferation through suppressing miR-205 and promoting SMAD4 expression in osteosarcoma.Oncotarget · 2017Article
- MicroRNA-138 directly targets TNFAIP8 and acts as a tumor suppressor in osteosarcoma.Experimental and therapeutic medicine · 2017Article
- miRNA-205 targets VEGFA and FGF2 and regulates resistance to chemotherapeutics in breast cancer.Cell death & disease · 2016Article
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Authors and funding
8 authors.
Funding
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Abstract
backgroundOsteosarcoma (OS) is the most common primary bone malignancy in children and young adults. MiR-205 has been reported to be negatively correlated with the proliferation and metastasis of many types of cancer, while its effects on the malignant phenotype of OS are unclear.
methodsUsing TaqMan RT polymerase chain reaction analysis, we firstly explored the expression of miR-205 in a panel of OS cell lines. As the expression of miR-205 was significantly decreased in these cell lines, we sought to compensate for its loss by transfection of exogenous miR-205 mimic into MG-63 cells. To further understand the role of miR-205 in OS, we investigated the effects of miR-205 on the proliferation, migration, and invasion of MG-63 cells, and further explored the mechanisms that might be involved.
resultsWe found that miR-205 was consistently suppressed in OS cells when compared with the normal human osteoblast (NHOst) cell line. Restored expression of miR-205 in the OS (MG-63) cell line significantly inhibited cell proliferation, migration, and invasion. Moreover, bioinformatic prediction suggested that vascular endothelial growth factor A (VEGFA) was the target oncogene for miR-205 in OS cells. Further quantitative RT polymerase chain reaction and Western blot assays identified that overexpression of miR-205 suppressed expression of VEGFA mRNA and protein. Restored expression of VEGFA in MG-63 cells previously treated with miR-205 mimic could partially abolish miR-205-mediated suppression of proliferation and invasion of these cells.
conclusionCollectively, these data suggest that miR-205 might function as a tumor suppressor in OS by, at least partially, targeting VEGFA.
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