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TRANSIENT APOPTOSIS ELICITED BY INSULIN IN SERUM‐STARVED GLIOMA CELLS INVOLVES Fas/Fas‐L AND Bcl‐2
Author(s) -
Yang BeiChang,
Wang YuhSheng,
Wang ChengHsin,
Lin HsiHui,
Tang MingJer,
Yang TsaeLian
Publication year - 1999
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1006/cbir.1999.0408
Subject(s) - apoptosis , fas receptor , glioma , insulin , biology , programmed cell death , gene expression , cancer research , microbiology and biotechnology , gene , chemistry , endocrinology , genetics
The expression of fas gene in glioma cells varies with growth stage. When insulin‐elicited transient apoptosis of glioma cells was in progress, the expression of fas gene increased at both transcriptional and translational levels. In contrast, the expression of fas‐L gene in glioma cells remained constant. Apoptosis occurred in the cells having high level of surface Fas protein. When the expression of Fas‐L in U‐373MG cells was suppressed by ribozyme, the insulin‐elicited transient apoptosis vanished. Overexpression of Bcl‐2 in U‐373MG cells did not alter significantly the cell cycle progression and the expression of fas gene. However, these cells were resistant to insulin‐trigged death. Therefore, insulin‐elicited apoptosis involved Fas‐related death signal, and which could be prevented by the protective effect of Bcl‐2.