Distinct Cellular Calcium Metabolism in Radiation-sensitive RKO Human Colorectal Cancer Cells
The Korean Journal of Physiology and Pharmacology
;
: 509-516, 2014.
Article
in English
| WPRIM
| ID: wpr-727692
ABSTRACT
Radiation therapy for variety of human solid tumors utilizes mechanism of cell death after DNA damage caused by radiation. In response to DNA damage, cytochrome c was released from mitochondria by activation of pro-apoptotic Bcl-2 family proteins, and then elicits massive Ca2+ release from the ER that lead to cell death. It was also suggested that irradiation may cause the deregulation of Ca2+ homeostasis and trigger programmed cell death and regulate death specific enzymes. Thus, in this study, we investigated how cellular Ca2+ metabolism in RKO cells, in comparison to radiation-resistant A549 cells, was altered by gamma (gamma)-irradiation. In irradiated RKO cells, Ca2+ influx via activation of NCX reverse mode was enhanced and a decline of [Ca2+]i via forward mode was accelerated. The amount of Ca2+ released from the ER in RKO cells by the activation of IP3 receptor was also enhanced by irradiation. An increase in [Ca2+]i via SOCI was enhanced in irradiated RKO cells, while that in A549 cells was depressed. These results suggest that gamma-irradiation elicits enhancement of cellular Ca2+ metabolism in radiation-sensitive RKO cells yielding programmed cell death.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
DNA Damage
/
Colorectal Neoplasms
/
Calcium
/
Cell Death
/
Cytochromes c
/
Inositol 1,4,5-Trisphosphate Receptors
/
Homeostasis
/
Metabolism
/
Mitochondria
Type of study:
Diagnostic study
Limits:
Humans
Language:
English
Journal:
The Korean Journal of Physiology and Pharmacology
Year:
2014
Type:
Article
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