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Negative cell cycle control of human T cells by β‐galactoside binding protein (βGBP): Induction of programmed cell death in leukaemic cells
Author(s) -
Novelli Francesco,
Allione Alessandra,
Wells Valerie,
Forni Guido,
Mallucci Livio
Publication year - 1999
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/(sici)1097-4652(199901)178:1<102::aid-jcp13>3.0.co;2-6
Subject(s) - microbiology and biotechnology , cell , programmed cell death , cell cycle , chemistry , biology , apoptosis , biochemistry
The cell cycle is negatively regulated by diverse molecular events which originate in part from the interaction of secreted proteins with specific cell surface receptors. By exerting negative control on cell proliferation, these factors can help maintain cell number balance both through growth restraints and the induction of apoptosis and may thus contribute to prevent or control tumourigenesis. Here we report that βGBP, a negative growth factor which controls transition from S phase into G 2 , causes an S/G 2 growth arrest in both normal and leukaemic T cells. However, in leukaemic T cells but not in normal T lymphocytes, growth arrest is followed by apoptosis. Analysis of possible mechanisms of induction of apoptosis does not support Fas and Fas L as having a main role but points instead to Bcl‐2 and Bax. The induction of apoptosis in leukaemic T cells is characterised by the decrease of Bcl‐2 and consequent predominance of Bax. By contrast, in the normal T cells, which do not enter apoptosis, the quantitative relationship of Bcl‐2 to Bax remains unchanged. The ability of βGBP to selectively induce apoptosis in leukaemic cells suggests that βGBP may play a role in cancer surveillance and that its use has potential therapeutic implications. J Cell Physiol 178:102–108, 1999. © 1999 Wiley‐Liss, Inc.