2004 Fiscal Year Final Research Report Summary
Study on the abnormal signal transduction of TGF-β1 in Epstein-Barr virus positive cell lines.
| Project/Area Number |
15390150
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Virology
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| Research Institution | National University Corporation Tottori University |
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Principal Investigator |
SAIRENJI Takeshi National University Corporation Tottori University, Faculty of Medicine, Department of Biomedical Sciences, Professor, 医学部, 教授 (10117351)
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| Co-Investigator(Kenkyū-buntansha) |
SATOH Yukio National University Corporation Tottori University, Faculty of Medicine, Department of Biomedical Sciences, Research Associate, 医学部, 助手 (70144657)
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| Project Period (FY) |
2003 – 2004
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| Keywords | Epstein-Barr virus (EBV) / TGF-β1 / TGF-β receptor / TGF-β1 signal / Burkitt's lymphoma / EBV oncogenesis / EBV reactivation / siRNA |
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| Research Abstract |
(1).Loss of Functional Transforming Growth Factor(TGF)-β Type II Receptor Results in Insensitivity to TGF-β1 in Epstein-Barr Virus-positive Burkitt's Lymphoma Cell Line Akata (submitted).
We analyzed the effect of TGF-β1 on the cell growth and Epstein-Barr virus(EBV) reactivation in six Burkitt's lymphoma cell lines. TGF-β1 induced cell growth inhibition and EBV reactivation in these cell lines but did not in Akata cells. To elucidate the mechanism of TGF-β1 unresponsiveness in Akata cells, we studied the expression of TGF-β receptors and the intracellular signaling molecules Smads. All cell lines expressed TGF-β type I receptor, Smad2, Smad3 and Smad4. TGF-β type II receptor (R-II) was expressed in all cell lines except Akata cells. Introduction of the TGF-β R-II into Akata cells results in sensitivity to TGF-β1-mediated growth inhibition, and EBV reactivation. To test a possibility to the transcriptional repression of the TGF-β R-II gene in Akata cells, the effect of histone deacetyla
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tion (HDAC) inhibitor, trichostatin A(TSA) was examined. The expression of TGF-β R-II in Akata cells was induced by TSA treatment. These results suggest that the defect in the TGF-β1 response in Akata cells is caused by the lack of TGF-β R-II and the alteration of HDAC may be involved in the loss of TGF-β R-II in the cells.
(2).Mechanism for induction of hydroxyurea(HU) resistance and loss of latent EBV genome in HU-treated BL cell line Raji (J.Med.Virol.70: 224,2003;J.Med.Virol.73:589,2004).
(3).Inhibition of EBV reactivation by short interfering RNAs targeting p38 mitogen activated protein kinase or c-Myc in EBV-positive epithelial cells (J.Virol.78:11798,2004).
(4).Characterization of Epstein-Barr virus infection in a human signet ring cell gastric carcinoma cell line HSC-39. (Microbes and Infection 6:429,2004).
(5).Diagnostic evaluation of 2',5'-oligoadenylate synthetase activities and antibodies against Epatein-Barr virus and Coxiella burnetii in patients with choronic fatigue syndrome in Japan (Microbes and Infection 5:1096,(2003). Less
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[Journal Article] Epstein-Barr virus infected malignant NK/T-cell lymphoma in a patient with hypersensitivity to mosquito bites.2004
Author(s)
Kase S., Adachi H., Osaki M., Murakami M., Sairenji T., Hashimoto K., Teramoto H., Yamamoto S., Makino H., Shimizu E., Watanabe T., Ohasawa T., Hagari Y., Mihara M., Ito H.
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Journal Title
Int.J.Surg.Pathol. 12
Pages: 265-272
Description
「研究成果報告書概要(欧文)」より
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[Journal Article] Diagnostic evaluation of 2',5'-oligoadenylate synthetase activities and antibodies against Epstein-Barr virus and Coxiella burnetii in patients with choronic fatigue syndrome in Japan.2003
Author(s)
Ikuta K, Yamada T, Shimomura T, Kuratsune H, Kawahara R, Ikawa S, Ohnishi E, Sokawa Y, Fukushi H, Hirai K, Watanabe Y, Kurata T, Kitani T, Sairenji T
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Journal Title
Microbes and Infection 5
Pages: 1096-1102
Description
「研究成果報告書概要(欧文)」より
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