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Induction of Epstein-Barr virus (EBV) reactivation in Raji cells by doxorubicin and cisplatin.
Anticancer Res. 2002 Nov-Dec; 22(6C):4065-71.AR

Abstract

BACKGROUND

Epstein-Barr virus (EBV) can be activated in B-lymphoid cells to enter the lytic cycle by various kinds of stimuli, including 12-O-tetradecanoylphorbol-1 3-acetate (TPA), butyric acid, calcium ionophore A23187, transforming growth factor-beta and anti-immunoglobulin crosslinking. EBV reactivation has been clinically observed in patients receiving systemic chemotherapy. This study sought in vitro evidence to suggest whether anticancer drugs may directly contribute to the EBV reactivation.

MATERIALS AND METHODS

Raji cells, an EBV-containing Burkitt's lymphoma cell line, were used as the experimental model. TPA served as a positive control for chemical induction of EBV reactivation. Expression of the BZLF1 transcript of EBV and its encoded protein, ZEBRA, were examined by real-time quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and flow cytometry, respectively. Transactivation activity of ZEBRA was further assessed by a luciferase reporter assay of EBV DR-promoter activity and a flow cytometry assay assessing the endogenous expression of EA-D (BMRFl).

RESULTS

Doxorubicin and cisplatin, two commonly used anticancer agents, induced a dose-dependent up-regulation of BZLF1 mRNA and ZEBRA protein. The luciferase reporter activity and the expression of endogenous EA-D protein, also increased by doxorubicin and cisplatin, indicated an up-regulation of the transactivating activity of ZEBRA.

CONCLUSION

These data indicate that cytotoxic anticancer drugs may up-regulate the expression and the transactivating activity of BZLF1, and suggest that systemic chemotherapy may be a risk factor for EBV reactivation in patients with EBV-associated malignancies.

Authors+Show Affiliations

Department of Oncology, National Taiwan University Hospital, Cancer Research Center, National Taiwan University College of Medicine, Taipei, Taiwan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12553034

Citation

Hsu, Chih-Hung, et al. "Induction of Epstein-Barr Virus (EBV) Reactivation in Raji Cells By Doxorubicin and Cisplatin." Anticancer Research, vol. 22, no. 6C, 2002, pp. 4065-71.
Hsu CH, Hergenhahn M, Chuang SE, et al. Induction of Epstein-Barr virus (EBV) reactivation in Raji cells by doxorubicin and cisplatin. Anticancer Res. 2002;22(6C):4065-71.
Hsu, C. H., Hergenhahn, M., Chuang, S. E., Yeh, P. Y., Wu, T. C., Gao, M., & Cheng, A. L. (2002). Induction of Epstein-Barr virus (EBV) reactivation in Raji cells by doxorubicin and cisplatin. Anticancer Research, 22(6C), 4065-71.
Hsu CH, et al. Induction of Epstein-Barr Virus (EBV) Reactivation in Raji Cells By Doxorubicin and Cisplatin. Anticancer Res. 2002 Nov-Dec;22(6C):4065-71. PubMed PMID: 12553034.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Induction of Epstein-Barr virus (EBV) reactivation in Raji cells by doxorubicin and cisplatin. AU - Hsu,Chih-Hung, AU - Hergenhahn,Manfred, AU - Chuang,Shuan-En, AU - Yeh,Pei-Yen, AU - Wu,Ta-Chung, AU - Gao,Ming, AU - Cheng,Ann-Lii, PY - 2003/1/30/pubmed PY - 2003/3/8/medline PY - 2003/1/30/entrez SP - 4065 EP - 71 JF - Anticancer research JO - Anticancer Res VL - 22 IS - 6C N2 - BACKGROUND: Epstein-Barr virus (EBV) can be activated in B-lymphoid cells to enter the lytic cycle by various kinds of stimuli, including 12-O-tetradecanoylphorbol-1 3-acetate (TPA), butyric acid, calcium ionophore A23187, transforming growth factor-beta and anti-immunoglobulin crosslinking. EBV reactivation has been clinically observed in patients receiving systemic chemotherapy. This study sought in vitro evidence to suggest whether anticancer drugs may directly contribute to the EBV reactivation. MATERIALS AND METHODS: Raji cells, an EBV-containing Burkitt's lymphoma cell line, were used as the experimental model. TPA served as a positive control for chemical induction of EBV reactivation. Expression of the BZLF1 transcript of EBV and its encoded protein, ZEBRA, were examined by real-time quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and flow cytometry, respectively. Transactivation activity of ZEBRA was further assessed by a luciferase reporter assay of EBV DR-promoter activity and a flow cytometry assay assessing the endogenous expression of EA-D (BMRFl). RESULTS: Doxorubicin and cisplatin, two commonly used anticancer agents, induced a dose-dependent up-regulation of BZLF1 mRNA and ZEBRA protein. The luciferase reporter activity and the expression of endogenous EA-D protein, also increased by doxorubicin and cisplatin, indicated an up-regulation of the transactivating activity of ZEBRA. CONCLUSION: These data indicate that cytotoxic anticancer drugs may up-regulate the expression and the transactivating activity of BZLF1, and suggest that systemic chemotherapy may be a risk factor for EBV reactivation in patients with EBV-associated malignancies. SN - 0250-7005 UR - https://www.unboundmedicine.com/medline/citation/12553034/Induction_of_Epstein_Barr_virus__EBV__reactivation_in_Raji_cells_by_doxorubicin_and_cisplatin_ DB - PRIME DP - Unbound Medicine ER -