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Hyperthermia in combination with oxidative stress induces autophagic cell death in HT‐29 colon cancer cells
Author(s) -
Chen Fei,
Wang ChiaChi,
Kim Eugene,
Harrison Lawrence E.
Publication year - 2008
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2008.02.010
Subject(s) - autophagy , programmed cell death , vacuole , autophagosome , apoptosis , microbiology and biotechnology , hyperthermia , cytoplasm , chemistry , organelle , oxidative stress , cell , viability assay , cancer research , biology , biochemistry , paleontology
The purpose of this study was to evaluate the mechanism of ROS‐induced hyperthermic cell death in a colon cancer cell line. HT‐29 colon cancer cells were exposed to heat (43 °C) in the presence of tert ‐butyl hydroperoxide ( t ‐BOOH). t ‐BOOH combined with hyperthermia significantly decreased cell viability as compared with t ‐BOOH or hyperthermia alone. This decrease in cell numbers was associated with retardation in the S phase transit and not through apoptosis. Cell death was noted to be accompanied by specific features characteristic of autophagy: the presence of cytoplasmic autophagic vacuoles; autophagosome membrane association of microtubule‐associated protein light chain 3; accumulation of acidic vesicular organelles; and increased incorporation of MDC in the autophagosome. Thermal sensitization through modulation of cellular ROS may represent a novel approach to increase the efficacy of hyperthermia as an anticancer modality.