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已发表论文
miR-205 通过靶向 VEGFA 抑制人体骨肉瘤 MG-63 细胞的增殖和迁移能力
Authors Wang L, Shan M, Yang F, Liu Y, Qi H, Zhou L, Qiu L, Li Y
Received 31 December 2014
Accepted for publication 26 March 2015
Published 16 September 2015 Volume 2015:8 Pages 2635—2642
DOI http://dx.doi.org/10.2147/OTT.S80088
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 6
Editor who approved publication: Dr Faris Farassati
Background: Osteosarcoma (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.
Methods: Using 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.
Results: We 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.
Conclusion: Collectively, these data suggest that miR-205 might function as a tumor suppressor in OS by, at least partially, targeting VEGFA .
Keywords: miR-205, osteosarcoma, vascular endothelial growth factor A, metastasis
Methods: Using 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.
Results: We 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.
Conclusion: Collectively, these data suggest that miR-205 might function as a tumor suppressor in OS by, at least partially, targeting VEGFA .
Keywords: miR-205, osteosarcoma, vascular endothelial growth factor A, metastasis
