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Resistance of Ehrlich tumor cells to apoptosis can be due to accumulation of heat shock proteins
Author(s) -
Gabai Vladimir L.,
Zamulaeva Irina V.,
Mosin Alexei F.,
Makarova Yulia M.,
Mosina Vera A.,
Budagova Karina R.,
Malutina Yana V.,
Kabakov Alexander E.
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)01152-5
Subject(s) - cycloheximide , heat shock protein , apoptosis , microbiology and biotechnology , programmed cell death , in vivo , hsp70 , vinblastine , ehrlich ascites carcinoma , biology , cytosol , endogeny , chemistry , protein biosynthesis , biochemistry , enzyme , genetics , chemotherapy , gene
Previously we have found that stationary Ehrlich ascites carcinoma (EAC) cells in vivo accumulated heat shock proteins (HSPs) and became resistant to necrotic heath induced by prolonged energy deprivation of hyperthermia. Here we report that apoptotic death induced by nutrient starvation, transient ATP depletion, heat shock and a microtubule‐disrupting drug, vinblastine, was also suppressed in stationary EAC cells comparing with exponential cells. When exponential (sensitive) cells were subjected to short‐term heating with recovery to accumulate inducible form of HSP70, they also became resistant to all of the employed apoptosis‐inducing exposures, and an inhibitor of cytosolic protein synthesis, cycloheximide, prevented acquisition of the resistance. It is suggested that in vivo accumulation of HSPs in stationary tumor cells can be endogenous protective device against apoptotic death induced by starvation or some anticancer treatments.