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Transfer of suppressor of cytokine signaling 3 by an oncolytic adenovirus induces potential antitumor activities in hepatocellular carcinoma.

Transfer of suppressor of cytokine signaling 3 by an oncolytic adenovirus induces potential antitumor activities in hepatocellular carcinoma. Research Abstract Details 

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  • Transfer of suppressor of cytokine signaling 3 by an oncolytic adenovirus induces potential antitumor activities in hepatocellular carcinoma. Abstract Text:

    qiang cuiQiang Cui,wei jiangWei Jiang,yingxin wangYingxin Wang,chen lvChen Lv,jingjing luoJingjing Luo,wei zhangWei Zhang,fang linFang Lin,yuexiang yinYuexiang Yin,rong caiRong Cai,ping weiPing Wei,cheng qianCheng Qian,qiang cuiQiang Cui,wei jiangWei Jiang,yingxin wangYingxin Wang,chen lvChen Lv,jingjing luoJingjing Luo,wei zhangWei Zhang,fang linFang Lin,yuexiang yinYuexiang Yin,rong caiRong Cai,ping weiPing Wei,cheng qianCheng Qian,

    The constitutive activation of signal transducer and activator of transcription 3 (STAT3) participates in carcinogenesis through up-regulation of genes encoding apoptosis inhibitors and cell cycle regulators, such as Bcl-xL, cyclins D1 and D2, and c-myc. Suppressor of cytokine signaling 3 (SOCS3) is one of the negative regulators of cytokine signaling and is frequently silenced in diverse cancers. In this study, we explored whether restoration of SOCS3 by oncolytic adenoviral vectors could inhibit the constitutive activation of the Janus kinase/STAT pathway and suppress tumor growth. Our data showed that SOCS3 was down-expressed in all liver tumor cell lines. The incorporation of SOCS3 or SOCS3 fused with cell-penetrating peptides (cpp-SOCS3) did not alter adenoviral replication selectively in liver tumor cells. The infection of cells with adenovirus CN305 (AdCN305)-SOCS3 and AdCN305-cpp-SOCS3 resulted in dramatic cytotoxicity in liver tumor cells. However, no cytotoxic effect was observed in normal cells infected with these vectors. Infection of liver tumor cells with AdCN305-SOCS3 and AdCN305-cpp-SOCS3 resulted in nearly complete inhibition of STAT3 phosphorylation and down-regulation of cyclin D1 and Bcl-xL. Treatment of the established tumor by AdCN305-SOCS3 and AdCN305-cpp-SOCS3 caused significant suppression of tumor growth. The suppression of tumor growth was due to the inhibition of STAT3 phosphorylation and induction of tumor cell death. Conclusion: This study suggests that transfer of SOCS3 by an oncolytic adenovirus represents a potent approach for cancer therapy. (HEPATOLOGY 2007.).

    Transfer of suppressor of cytokine signaling 3 by an oncolytic adenovirus induces potential antitumor activities in hepatocellular carcinoma. Publishing Authors By Initials

    q cuiQ Cui,w jiangW Jiang,y wangY Wang,c lvC Lv,j luoJ Luo,w zhangW Zhang,f linF Lin,y yinY Yin,r caiR Cai,p weiP Wei,c qianC Qian,q cuiQ Cui,w jiangW Jiang,y wangY Wang,c lvC Lv,j luoJ Luo,w zhangW Zhang,f linF Lin,y yinY Yin,r caiR Cai,p weiP Wei,c qianC Qian,

    For similar abstracts research abstracts see: abstracts research

    PUBMED ID PMID:

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    Transfer of suppressor of cytokine signaling 3 by an oncolytic adenovirus induces potential antitumor activities in hepatocellular carcinoma. Journal Published:

    PUBLICATION TYPE: Journal Article

    Journal: Hepatology (Baltimore, Md.)

    VOLUME: 47

    Page Numbers: 105-12

    Journal Abbreviation: Hepatology

    ISSN: 1527-3350

    DAY: 2

    MONTH: Jan

    YEAR: 2008

    Transfer of suppressor of cytokine signaling 3 by an oncolytic adenovirus induces potential antitumor activities in hepatocellular carcinoma. Information

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    LANGUAGE: eng

    NlmUniqueID: 8302946

    Transfer of suppressor of cytokine signaling 3 by an oncolytic adenovirus induces potential antitumor activities in hepatocellular carcinoma. Keywords Mesh Terms:

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    Grant and Affiliation Information for Transfer of suppressor of cytokine signaling 3 by an oncolytic adenovirus induces potential antitumor activities in hepatocellular carcinoma.

    AFFILIATION: Xinyuan Institute of Medicine and Biotechnology, School of Life Sciences, Zhejiang Sci-Tech University, Hangzhou, China.

    Country: United States

    United States Research PublicationUnited States Research Publication

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    MEDLINETA: Hepatology

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