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MPA increases idarubicin‐induced apoptosis in chronic lymphatic leukaemia cells via caspase‐3
Author(s) -
Florio Salvatore,
Crispino Luca,
Ciarcia Roberto,
Vacca Giovanni,
Pagnini Ugo,
Matteis Andrea de,
Pacilio Carmen,
D'Andrilli Giuseppina,
Kumar Christine,
Giordano Antonio
Publication year - 2003
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.10556
Subject(s) - apoptosis , propidium iodide , chemistry , caspase 3 , caspase 9 , caspase , caspase 8 , microbiology and biotechnology , idarubicin , cancer research , medicine , biology , programmed cell death , biochemistry , myeloid leukemia , cytarabine
The caspase family of protease is speculated to have a crucial role in apoptosis. The effect of treatment with Idarubicin (IDA) and Medroxyprogesterone acetate (MPA), used alone or in combination, on the activation of Caspase‐3 in canine Chronic Lymphatic Leukaemia (CLL) cells was investigated, in order to clarify the mechanism of chemo‐ and hormone‐therapy mediated apoptosis. Caspase activity was determined by a quantitative fluorimetric assay. Apoptosis was monitored by propidium iodide (PI) and nucleosomes assay. Treatment of CLL cells for 24 h with MPA 5 μM did not significantly activate caspase‐3 but its activity was increased almost 5‐fold more with IDA 1 μM ( P < 0.05) than control. Treatment of CLL cells with IDA 1 μM in equimolecular association with MPA was able to increase the activation of caspase‐3 induced by IDA of the 61.2% ( P < 0.05) in comparison with IDA alone. The activation of caspase‐3 was confirmed evaluating apoptosis by PI and nucleosomes assay. Furthermore, both caspase‐3 activation and apoptosis triggered by IDA alone or in combination with MPA were significantly inhibited by specific caspase‐3 inhibitor AC‐DEVD‐CMK. These findings provide an explanation for IDA and MPA induced‐apoptosis mechanism. J. Cell. Biochem. 89: 747–754, 2003. © 2003 Wiley‐Liss, Inc.