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Cancer Investigation Volume 30, 2012 - Issue 4
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CELLULAR AND MOLECULAR BIOLOGY

Cisplatin Disrupts the Latency of Human Herpesvirus 8 and Induces Apoptosis in Primary Effusion Lymphoma Cells

Yi-Fen WangDepartment of Medical Laboratory Sciences and Biotechnology, Fooyin-University, Kaohsiung, Taiwan, ROC,Correspondence[email protected]
,
Yee-Hsuan ChiouDepartment of Pediatrics, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, ROC
,
Lin-Yu WangDepartment of Medical Laboratory Sciences and Biotechnology, Fooyin-University, Kaohsiung, Taiwan, ROC,
,
Su-Ting ChangDepartment of Medical Laboratory Sciences and Biotechnology, Fooyin-University, Kaohsiung, Taiwan, ROC,
,
Huey-Wen ShyuDepartment of Medical Laboratory Sciences and Biotechnology, Fooyin-University, Kaohsiung, Taiwan, ROC,
,
Chang-Yu ChenDepartment of Medical Laboratory Sciences and Biotechnology, Fooyin-University, Kaohsiung, Taiwan, ROC,
,
Kuan-Hua LinDepartment of Medical Laboratory Sciences and Biotechnology, Fooyin-University, Kaohsiung, Taiwan, ROC,
&
Miao-Chen ChouDepartment of Medical Laboratory Sciences and Biotechnology, Fooyin-University, Kaohsiung, Taiwan, ROC,
 show all
Pages 268-274 | Published online: 05 Apr 2012
 
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Abstract

Human herpesvirus 8 (HHV8) is the etiologic agent for primary effusion lymphoma (PEL). The aim of this study is to investigate the effects of cisplatin on the PEL cells. Cisplatin treatment induced apoptosis and inhibited the growth of PEL cells, and the effect was more profound in the HHV8-positive lymphoma cells compared with the EBV-positive lymphoma cells. Cisplatin treatment decreased the expression of HHV8 latent genes and activated p53 at serine 15 in PEL cells. Our results indicate that cisplatin can disrupt HHV8 latency and induce reactivation of p53 and highly selective treatment modality for this virally induced lymphoma.

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