The Experts below are selected from a list of 5736 Experts worldwide ranked by ideXlab platform
Chuanju Liu - One of the best experts on this subject based on the ideXlab platform.
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ifi16 inhibits Tumorigenicity and cell proliferation of bone and Cartilage Tumor cells
Frontiers in Bioscience, 2007Co-Authors: Yan Zhang, Ronald D Howell, Daniel T Alfonso, Li Kong, James C Wittig, Chuanju LiuAbstract:IFI16 is a member of the interferon-inducible p200-protein family, capable of modulating cell proliferation, and cellular senescence. In this study, these effects of IFI16 were studied in Tumor cells derived from bone and Cartilage. The level of IFI16 was markedly lower in human osteosarcomas as compared with its level in normal bone. Overexpression of functional IFI16 in human osteosarcoma and chondrosarcoma cell lines markedly inhibited colony formation, and significantly inhibited cell growth, an effect that could be reversed by introduction of gene specific siRNA into Tumor cells. These inhibitory effects of IFI16 were associated with upregulation of p21 and inhibition of cyclin E, cyclin D1, c-Myc and Ras. In addition, ectopic expression of IFI16 in Tumor cells increased senescence-associated beta-galactosidase and induced a senescence-like phenotype. In view of such effects, IFI16 might be a suitable target for therapeutic intervention in osteosarcoma and chondrosarcoma.
Yan Zhang - One of the best experts on this subject based on the ideXlab platform.
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ifi16 inhibits Tumorigenicity and cell proliferation of bone and Cartilage Tumor cells
Frontiers in Bioscience, 2007Co-Authors: Yan Zhang, Ronald D Howell, Daniel T Alfonso, Li Kong, James C Wittig, Chuanju LiuAbstract:IFI16 is a member of the interferon-inducible p200-protein family, capable of modulating cell proliferation, and cellular senescence. In this study, these effects of IFI16 were studied in Tumor cells derived from bone and Cartilage. The level of IFI16 was markedly lower in human osteosarcomas as compared with its level in normal bone. Overexpression of functional IFI16 in human osteosarcoma and chondrosarcoma cell lines markedly inhibited colony formation, and significantly inhibited cell growth, an effect that could be reversed by introduction of gene specific siRNA into Tumor cells. These inhibitory effects of IFI16 were associated with upregulation of p21 and inhibition of cyclin E, cyclin D1, c-Myc and Ras. In addition, ectopic expression of IFI16 in Tumor cells increased senescence-associated beta-galactosidase and induced a senescence-like phenotype. In view of such effects, IFI16 might be a suitable target for therapeutic intervention in osteosarcoma and chondrosarcoma.
Jinzhi Wang - One of the best experts on this subject based on the ideXlab platform.
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gene silencing of usp1 by lentivirus effectively inhibits proliferation and invasion of human osteosarcoma cells
International Journal of Oncology, 2016Co-Authors: Ning Zhong, Youping Deng, Lin Xu, Z Jiang, Hongwei Wang, Jinzhi WangAbstract:Osteosarcoma is the most frequent malignant bone Tumor, affecting the extremities of adolescents and young adults. Ubiquitin-specific protease 1 (USP1) plays a critical role in many cellular processes including proteasome degradation, chromatin remodeling and cell cycle regulation. In the present study, we discovered that USP1 was overexpressed in 26 out of 30 osteosarcoma tissues compared to Cartilage Tumor tissues and normal bone tissues. We then constructed a lentiviral vector mediating RNA interference (RNAi) targeting USP1 and demonstrated that it significantly suppressed the mRNA and protein expression of the USP1 gene in U2OS cells. Knockdown of USP1 inhibited the growth and colony-forming, as well as significantly reduced the invasiveness of U2OS cells. Western blot analysis indicated that suppression of USP1 downregulated the expression of many proteins including SIK2, MMP-2, GSK-3β, Bcl-2, Stat3, cyclin E1, Notch1, Wnt-1 and cyclin A1. Most of these proteins are associated with Tumor genesis and development. RNAi of SIK2 significantly decreased SIK2 protein expression and inhibited the ability of forming colonies, as well as induced apoptosis and reduced the invasiveness of U2OS cells. Collectively, our results suggest that silencing USP1 inhibits cell proliferation and invasion in U2OS cells. Therefore, USP1 may provide a novel therapeutic target for the treatment of osteosarcoma.
Daniel T Alfonso - One of the best experts on this subject based on the ideXlab platform.
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ifi16 inhibits Tumorigenicity and cell proliferation of bone and Cartilage Tumor cells
Frontiers in Bioscience, 2007Co-Authors: Yan Zhang, Ronald D Howell, Daniel T Alfonso, Li Kong, James C Wittig, Chuanju LiuAbstract:IFI16 is a member of the interferon-inducible p200-protein family, capable of modulating cell proliferation, and cellular senescence. In this study, these effects of IFI16 were studied in Tumor cells derived from bone and Cartilage. The level of IFI16 was markedly lower in human osteosarcomas as compared with its level in normal bone. Overexpression of functional IFI16 in human osteosarcoma and chondrosarcoma cell lines markedly inhibited colony formation, and significantly inhibited cell growth, an effect that could be reversed by introduction of gene specific siRNA into Tumor cells. These inhibitory effects of IFI16 were associated with upregulation of p21 and inhibition of cyclin E, cyclin D1, c-Myc and Ras. In addition, ectopic expression of IFI16 in Tumor cells increased senescence-associated beta-galactosidase and induced a senescence-like phenotype. In view of such effects, IFI16 might be a suitable target for therapeutic intervention in osteosarcoma and chondrosarcoma.
Li Kong - One of the best experts on this subject based on the ideXlab platform.
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ifi16 inhibits Tumorigenicity and cell proliferation of bone and Cartilage Tumor cells
Frontiers in Bioscience, 2007Co-Authors: Yan Zhang, Ronald D Howell, Daniel T Alfonso, Li Kong, James C Wittig, Chuanju LiuAbstract:IFI16 is a member of the interferon-inducible p200-protein family, capable of modulating cell proliferation, and cellular senescence. In this study, these effects of IFI16 were studied in Tumor cells derived from bone and Cartilage. The level of IFI16 was markedly lower in human osteosarcomas as compared with its level in normal bone. Overexpression of functional IFI16 in human osteosarcoma and chondrosarcoma cell lines markedly inhibited colony formation, and significantly inhibited cell growth, an effect that could be reversed by introduction of gene specific siRNA into Tumor cells. These inhibitory effects of IFI16 were associated with upregulation of p21 and inhibition of cyclin E, cyclin D1, c-Myc and Ras. In addition, ectopic expression of IFI16 in Tumor cells increased senescence-associated beta-galactosidase and induced a senescence-like phenotype. In view of such effects, IFI16 might be a suitable target for therapeutic intervention in osteosarcoma and chondrosarcoma.