PKC isoform selectivity and radiation-induced apoptosis of HepG2 cells.
- Author:
Qiong XIA
1
;
Chuan-gang LI
;
Ai-min SUN
;
Xue-lin ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; physiology; radiation effects; Hep G2 Cells; Humans; Isoenzymes; classification; metabolism; Protein Kinase C-alpha; metabolism; Protein Kinase C-delta; metabolism; Radiation Tolerance; Signal Transduction; drug effects; physiology
- From: Journal of Southern Medical University 2010;30(6):1376-1378
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the expressions of protein kinase C (PKC) isoforms in X-ray-exposed HepG2 cells and identify the PKC isoforms that induce radioresistance in HepG2 cells.
METHODSCultured HepG2 cells were divided into control group and 6 Gy radiation group for corresponding treatments. The fluorescence intensity (FI) and the percentage of positive cells were determined using flow cytometry.
RESULTSThe FI of PKCalpha and PKCdelta were 2.28 and 5.05 in the radiation group, respectively, significantly higher than those in the control group (P<0.05). The percentages of PKCalpha- and PKCdelta -positive cells were significantly higher in the radiation group than in the control group (P<0.05). The FI and the percentages of PKC zeta, gamma, epsilon, zeta positive cells were rather low and showed no significant differences between the two groups (P>0.05); PKCbeta expression was not detected in the two groups of cells. The apoptosis rates of the control and radiation groups were 1.73% and 20.90%, respectively.
CONCLUSIONPKCalpha and PKCdelta may be involved in protecting HepG2 cells from radiation-induced apoptosis.
