Fas ligand expression in glioblastoma cell lines and primary astrocytic brain tumors - PubMed (original) (raw)

Clinical Trial

Fas ligand expression in glioblastoma cell lines and primary astrocytic brain tumors

C Gratas et al. Brain Pathol. 1997 Jul.

Abstract

Fas/APO-1 (CD95) is a cell surface receptor that mediates apoptosis when it reacts with Fas ligand (FasL) or Fas antibody. We previously reported that Fas expression is predominantly induced in perinecrotic glioma cells, suggesting that Fas induction is associated with apoptosis and necrosis formation, a histological hallmark of glioblastomas. In this study, we assessed the expression of FasL in 10 glioblastoma cell lines and in 14 astrocytic brain tumors (three low-grade astrocytomas and 11 glioblastomas). Reverse transcriptase (RT)-PCR revealed that all glioblastoma cell lines and primary astrocytic brain tumors express FasL. Immunohistochemically, FasL was predominantly expressed on the plasma membrane of glioma cells. These results suggest that FasL expression is common in human astrocytic brain tumors and may cause apoptosis of glioma cells if Fas expression is induced.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Alderson MR, Tough TW, Davis Smith T, Braddy S, Falk B, Schooley KA, Goodwin RG, Smith CA, Ramsdell F, Lynch DH (1995) Fas ligand mediates activation‐induced cell death in human T lymphocytes. J Exp Med 181: 71–77. - PMC - PubMed
    1. Barker FG, Davis RL, Chang SM, Prados MD (1996) Necrosis as a prognostic factor in glioblastoma multiforme. Cancer 77: 1161–1166. - PubMed
    1. Bellgrau D, Gold D, Selawry H, Moore J, Franzusoff A, Duke RC (1995) A role for CD95 ligand in preventing graft rejection. Nature 377: 630–632. - PubMed
    1. Burger PC Scheithauer BW (1994) Tumors of the Central Nervous System. Armed Forces Institute of Pathology: Washington , DC .
    1. Cheng J, Liu C, Koopman WJ, Mountz JD (1995) Characterization of human Fas gene. Exon/intron organization and promoter region. J Immunol 154: 1239–1245. - PubMed

Publication types

MeSH terms

Substances

LinkOut - more resources