Distinct Cellular Calcium Metabolism in Radiation-sensitive RKO Human Colorectal Cancer Cells.
10.4196/kjpp.2014.18.6.509
- Author:
Yun Tai KIM
1
;
Soo Shin JO
;
Young Jun PARK
;
Myung Za LEE
;
Chang Kook SUH
Author Information
1. Department of Physiology and Biophysics, Inha University College of Medicine, Incheon 401-751, Korea. cksuh@inha.ac.kr
- Publication Type:Original Article
- Keywords:
A549 cells;
Inositol-1,4,5-triphosphate receptors;
Na+-Ca2+ exchanger;
RKO cells;
Store-operated Ca2+ influx
- MeSH:
Calcium*;
Cell Death;
Colorectal Neoplasms*;
Cytochromes c;
DNA Damage;
Homeostasis;
Humans;
Inositol 1,4,5-Trisphosphate Receptors;
Metabolism*;
Mitochondria
- From:The Korean Journal of Physiology and Pharmacology
2014;18(6):509-516
- CountryRepublic of Korea
- Language:English
-
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.
