Effect of transforming growth factor-β1 on the cell growth and Epstein-Barr virus reactivation in EBV-infected epithelial cell lines

被引：34

作者：

Fukuda, M

Ikuta, K

Yanagihara, K

Tajima, M

Kuratsune, H

Kurata, T

Sairenji, T ^{[1
]}

机构：

[1] Tottori Univ, Fac Med, Sch Life Sci, Dept Biosignaling, Yonago, Tottori 6838503, Japan

[2] Natl Canc Ctr, Res Inst, Cent Anim Lab, Tokyo 1040045, Japan

[3] Teikyo Univ, Sch Med, Cent Clin Lab, Tokyo 1738606, Japan

[4] Osaka Univ, Grad Sch Med, Dept Hematol & Oncol, Osaka 5658640, Japan

[5] Natl Inst Infect Dis, Dept Pathol, Tokyo 1628640, Japan

来源：

VIROLOGY | 2001年 / 288卷 / 01期

基金：

日本科学技术振兴机构;

关键词：

D O I：

10.1006/viro.2001.1071

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Transforming growth factor (TGF)-beta1 is a multifunctional cytokine that plays important roles in regulating cell growth and differentiation in many biological systems. In this study, we found that gastric tissue-derived Epstein-Barr virus (EBV)-infected epithelia[ cell lines GT38 and GT39 had resistance to TGF-beta1-mediated growth inhibition and apoptosis compared to a TGF-beta1 -susceptible gastric carcinoma cell line HSC-39. However, TGF-beta1 partially Induced EBV reactivation In GT38 and GT39 cells, as shown by the Induction of EBV immediate-early BZLF1 RNA and its protein product ZEBRA and early antigen-D. The expressions of TGF-beta receptor I and II were detected in GT38 and GT39 cells by Northern and Western blot analyses. Both cell lines spontaneously produced the TGF-beta1, which was sufficient for inhibiting cell growth of HSC-39 cells. Taken together, these data suggest that TGF-beta1 may be a key factor for EBV reactivation and selective growth of EBV-infected epithelial cells in vivo. (C) 2001 Academic Press.

引用

页码：109 / 118

页数：10

共 43 条

[1] ARVANITAKIS L, 1995, J IMMUNOL, V155, P1047
[2] Physicochemical Activation of Recombinant Latent Transforming Growth Factor-beta's 1, 2, and 3
Brownh, Peter D.
Wakefiel, Lalage M.
Levinson, Arthur D.
Sporn, Michael B.
[J]. GROWTH FACTORS, 1990, 3 (01) : 35 - 43
[3] POLYMORPHIC PROTEINS ENCODED WITHIN BZLF1 OF DEFECTIVE AND STANDARD EPSTEIN-BARR VIRUSES DISRUPT LATENCY
COUNTRYMAN, J
JENSON, H
SEIBL, R
WOLF, H
MILLER, G
[J]. JOURNAL OF VIROLOGY, 1987, 61 (12) : 3672 - 3679
[4] Direct binding of Smad3 and Smad4 to critical TGFβ-inducible elements in the promoter of human plasminogen activator inhibitor-type 1 gene
Dennler, S
Itoh, S
Vivien, D
ten Dijke, P
Huet, S
Gauthier, JM
[J]. EMBO JOURNAL, 1998, 17 (11) : 3091 - 3100
[5] ENDOGENOUS TGF-BETA CONTRIBUTES TO THE INDUCTION OF THE EBV LYTIC CYCLE IN 2 BURKITT-LYMPHOMA CELL-LINES
DIRENZO, L
ALTIOK, A
KLEIN, G
KLEIN, E
[J]. INTERNATIONAL JOURNAL OF CANCER, 1994, 57 (06) : 914 - 919
[6] FUKAYAMA M, 1994, LAB INVEST, V71, P73
[7] RESTORATION OF SURFACE IGM-MEDIATED APOPTOSIS IN AN ANTI-IGM-RESISTANT VARIANT OF WEHI-231 LYMPHOMA-CELLS BY HS1, A PROTEIN-TYROSINE KINASE SUBSTRATE
FUKUDA, T
KITAMURA, D
TANIUCHI, I
MAEKAWA, Y
BENHAMOU, LE
SARTHOU, P
WATANABE, T
[J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (16) : 7302 - 7306
[8] Nitric oxide down-regulates Epstein-Barr virus reactivation in epithelial cell lines
Gao, XR
Tajima, M
Sairenji, T
[J]. VIROLOGY, 1999, 258 (02) : 375 - 381
[9] TGF-beta signalling from cell membrane to nucleus through SMAD proteins
Heldin, CH
Miyazono, K
tenDijke, P
[J]. NATURE, 1997, 390 (6659) : 465 - 471
[10] Cell-to-cell contact as an efficient mode of Epstein-Barr virus infection of diverse human epithelial cells
Imai, S
Nishikawa, J
Takada, K
[J]. JOURNAL OF VIROLOGY, 1998, 72 (05) : 4371 - 4378

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