Resistance of Ehrlich tumor cells to apoptosis can be due to accumulation of heat shock proteins

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...

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Bibliographic Details
Published in:FEBS letters 1995-11, Vol.375 (1), p.21-26
Main Authors: Gabai, Vladimir L., Zamulaeva, Irina V., Mosin, Alexei F., Makarova, Yulia M., Mosina, Vera A., Budagova, Karina R., Malutina, Yana V., Kabakov, Alexander E.
Format: Article
Language:English
Subjects:
Adenosine Triphosphate - metabolism
Animals
Antineoplastic Agents, Phytogenic - pharmacology
Apoptosis
Apoptosis - drug effects
Apoptosis - physiology
Carcinoma, Ehrlich Tumor - metabolism
Carcinoma, Ehrlich Tumor - pathology
Carcinoma, Ehrlich Tumor - physiopathology
CCCP, carbonyl cyanide m-chlorophenylhydrazone
Cell Cycle - drug effects
Cell Cycle - physiology
Chromatin - drug effects
Chromatin - ultrastructure
DMEM, Dulbecco's modified Eagle's minimal essential medium
DNA fragmentation
DNA, Neoplasm - analysis
DNA, Neoplasm - isolation & purification
DNA, Neoplasm - metabolism
EAC, Ehrlich ascites carcinoma
Ehrlich ascites carcinoma
Electrophoresis, Agar Gel
Heat shock proteins
Heat-Shock Proteins - biosynthesis
Hot Temperature
HSP, heat shock protein
Mice
Mice, Inbred C57BL
Microtubules - drug effects
PBS, phosphate-buffered saline
Vinblastine - pharmacology
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Summary: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.
ISSN:0014-5793
1873-3468
DOI:10.1016/0014-5793(95)01152-5