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CM1 Ligation Induces Apoptosis via Fas-FasL Interaction in Ramos Cells, but via Down-regulation of Bcl-2 and Subsequent Decrease of Mitochondrial Membrane Potential in Raji Cells

  • Lee, Young-Sun (Department of Anatomy and Tumor Immunity Medical Research Center, Seoul National University College of Medicine) ;
  • Kim, Yeong-Seok (Department of Anatomy, Inje University College of Medicine) ;
  • Kim, Dae-Jin (Department of Anatomy and Tumor Immunity Medical Research Center, Seoul National University College of Medicine) ;
  • Hur, Dae-Young (Department of Anatomy, Inje University College of Medicine) ;
  • Kang, Jae-Seung (Department of Anatomy and Tumor Immunity Medical Research Center, Seoul National University College of Medicine) ;
  • Kim, Young-In (Department of Anatomy and Tumor Immunity Medical Research Center, Seoul National University College of Medicine) ;
  • Hahm, Eun-Sil (Department of Anatomy and Tumor Immunity Medical Research Center, Seoul National University College of Medicine) ;
  • Cho, Dae-Ho (Department of Life Science, Sookmyung Women's University) ;
  • Hwang, Young-Il (Department of Anatomy and Tumor Immunity Medical Research Center, Seoul National University College of Medicine) ;
  • Lee, Wang-Jae (Department of Anatomy and Tumor Immunity Medical Research Center, Seoul National University College of Medicine)
  • Published : 2006.06.30
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Abstract

Background: CM1 (Centrocyte/-blast Marker I) defined by a mAb developed against concanavalin-A activated PBMC, is expressed specifically on a subpopulation of centroblasts and centrocytes of human germinal center (GC) B cells. Burkitt lymphoma (BL) is a tumor consisting of tumor cells with the characteristics of GC B cell. Previously we reported that CM1 ligation with anti-CM1 mAb induced apoptosis in Ramos $(IgM^{high})$ and Raji $(IgM^{low})$ cells. Methods & Results: In the present study, we observed that CM1 ligation with anti-CM1 mAb induced Fas ligand and Fas expression in Ramos cells, but not in Raji cells. Furthermore, anti-Fas blocking antibody, ZB4, blocked CM1-mediated apoptosis effectively in Ramos cells, but not in Raji cells. Increased mitochondrial membrane permeabilization, which was measured by $DiOC_6$, was observed only in Raji cells. In contrast to no significant change of Bax known as pro-apoptotic protein, anti-apoptotic protein Bcl-2 was significantly decreased in Raji cells. In addition, we observed that CM1 ligation increased release of mitochondrial cytochrome c and upregulated caspase-9 activity in Raji cells. Conclusion: These results suggest that apoptosis induced by CM1-ligation is mediated by Fas-Fas ligand interaction in Ramos cells, whereas apoptosis is mediated by down-regulation of Bcl-2 and subsequent decrease of mitochondrial membrane potential in Raji cells.

Keywords

References

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