[The mechanism of MAb225 regulating radiosensitivity of Tca8113 cell].
OBJECTIVE
The objective of this study was to investigate the mechanism of MAb225 regulating radiosensitivity of Tca8113 cells.


METHODS
Tca8113 cells were treated with MAb225 of different concentrations. The apoptosis rate was analysed by FCM and bi-fluorescence stain, the repair of DNA damage after radiation was analysed by single cell gel electrophoresis, cells redistribution in each phase of cell cycle was analysed by FCM, and GSH level of cell were assessed by spectrophotometer.


RESULTS
Radiation alone (6 Gy) and MAb225 alone (0.5 microg/ml) produced a 2-fold induction of apoptosis respectively, whereas exposure to MAb225 (0.5 microg/ml) combination with 6 Gy of radiation induced apoptosis 5-6 fold, compared to untreated controls (F test). The length of comet tail of cells which treated with MAb225 was significantly longer than that of the control cells (t test, P<0.05). The percentage of cells in S phase was significantly decreased in MAb225 treated cells. Intracellular GSH level of MAb225 treated cells was significantly lower than that of untreated cells (t test, P<0.05).


CONCLUSIONS
MAb225 increased the radiosensitivity of Tca8113 cells by enhancing radiation-induced apoptosis, downregulating S phase percentage, inhibiting DNA repair after radiation and decreasing GSH level.
Wang
Ming-guo
MG
Department of Stomatology, Jinan Central Hospital, Jinan 250013, Shandong Province, China. wmgsh@163.com
Gao
Ping
P
Wang
Zhong-he
ZH
Cai
Yi-li
YL
Shan
Bao-zhong
BZ
D000911:Antibodies, Monoclonal; D017209:Apoptosis; D002453:Cell Cycle; D045744:Cell Line, Tumor; D004249:DNA Damage; D004260:DNA Repair; D005978:Glutathione; D006801:Humans; D011836:Radiation Tolerance / Q000187:drug effects* / Q000276:immunology*; D047888:Receptors, Tumor Necrosis Factor, Type I
D000911:Antibodies, Monoclonal; D047888:Receptors, Tumor Necrosis Factor, Type I; D005978:Glutathione