Tumor regression by expression of high physiological levels of EBV latent membrane protein 1

Yu Hua Hsieh, Hao Ping Liu, Szecheng J. Lo, Yu Sun Chang*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

Abstract

Induction of apoptosis in tumor cells is one of therapeutic strategies of cancer. Previous studies indicate that LMP-1 can act as governor of cell proliferation because overexpression of latent membrane protein 1 (LMP-1) of Epstein-Barr virus (EBV) inhibits cell proliferation. Here we demonstrate that overexpression of the NLMP-1, isolated from an EBV strain prominent in Taiwanese population, also possess the ability to induce apoptosis of cells, and inhibit CT-26 tumor growth in mice. Mapping studies indicate that NLMP-1 transmembrane domain is required for induction of cytotoxicity. Intratumoral delivery of vectors expressing NLMP-1 or its membrane domain via electroporation induces tumor tissue damage, suppresses tumor growth in mice, and prolongs the survival of treated animals. In addition, the membrane domain of NLMP-1 alone induces effects similar to those induced by cotreatment with NLMP-1 and IL-12. Tumor-free mice at 120 days after the initial treatments were further challenged with CT-26 tumor cells. No tumor growth was observed. Thus, NLMP-1, and more specifically the transmembrane domain of NLMP-1, may be promising new therapeutic agents for control of tumor growth.

Original languageEnglish
Pages (from-to)310-317
Number of pages8
JournalCancer Biology and Therapy
Volume5
Issue number3
DOIs
StatePublished - 03 2006

Keywords

  • Apoptosis
  • EBV
  • In vivo electroporation
  • LMP-1
  • Tumor growth inhibition

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