Salamatu S Mambula1, Stuart K Calderwood. 1. Division of Molecular and Cellular Biology, Department of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Abstract
PURPOSE: Heat shock protein 70 (HSP70) is released from tumour cells and stimulates a potent anti-tumour immune response. METHODS: This study examined the role of hyperthermia, including heating conditions from the fever range, the hyperthermia range and the thermal ablation range, in HSP70 release from prostate carcinoma cells. It has observed HSP70 release from human prostate carcinoma cell lines (PC-3 and LNCaP) treated with hyperthermia. RESULTS: The effects of hyperthermia were complex and appeared to involve at least two mechanisms for HSP70 release. Hyperthermia at 40 degrees C strongly stimulated HSP70 release by an active secretion pathway. However, as temperatures were increased, this rapid secretion pathway became progressively inhibited and by a temperature of 55 degrees C, active secretion was abolished. However, when cells exposed to these heating conditions were allowed to recover at 37 degrees C for 24 h after heating, HSP70 release was observed at the high ablation temperature range and this appeared to be related to a concomitant damage to the plasma membrane. CONCLUSIONS: Thus, at least two mechanisms contribute to HSP70 release during hyperthermia and the relative contribution from each pathway depends on the temperature conditions.
PURPOSE:Heat shock protein 70 (HSP70) is released from tumour cells and stimulates a potent anti-tumour immune response. METHODS: This study examined the role of hyperthermia, including heating conditions from the fever range, the hyperthermia range and the thermal ablation range, in HSP70 release from prostate carcinoma cells. It has observed HSP70 release from humanprostate carcinoma cell lines (PC-3 and LNCaP) treated with hyperthermia. RESULTS: The effects of hyperthermia were complex and appeared to involve at least two mechanisms for HSP70 release. Hyperthermia at 40 degrees C strongly stimulated HSP70 release by an active secretion pathway. However, as temperatures were increased, this rapid secretion pathway became progressively inhibited and by a temperature of 55 degrees C, active secretion was abolished. However, when cells exposed to these heating conditions were allowed to recover at 37 degrees C for 24 h after heating, HSP70 release was observed at the high ablation temperature range and this appeared to be related to a concomitant damage to the plasma membrane. CONCLUSIONS: Thus, at least two mechanisms contribute to HSP70 release during hyperthermia and the relative contribution from each pathway depends on the temperature conditions.