Radiosensitizing effect of apatinib on esophageal cancer cell line Kyse-150 / 中华放射医学与防护杂志
Chinese Journal of Radiological Medicine and Protection
; (12): 805-809,831, 2017.
Artigo
em Chinês
| WPRIM (Pacífico Ocidental)
| ID: wpr-669066
Biblioteca responsável:
WPRO
ABSTRACT
Objective To evaluate the radiosensitization effect of apatinib on esophageal cancer cell line Kyse-150, and to investigate the underlying mechanism. Methods Cells were divided into four groupscontrol group, apatinib treatment group, X-ray radiation group, and the combination group treated with X-rays plus apatinib. The effect of apatinib with different concentrations on the cell proliferative and radiosensitivity were evaluated by CCK-8 kit and colony formation assay. Flow cytometry method was adopted to detect the effect of apatinib on cell cycle progress and apoptosis induction. Results Apatinib inhibited the proliferation of Kyse-150 cells in time-and dose-dependent manners (r=0. 89-0. 96, P<0. 05). With the increase of apatinib concentration, D0, Dq and SF2 value of Kyse-150 cells decreased and SERD0 value increased. Compared with control group, apatinib alone group, and radiation alone group, the cell apoptosis rate significantly increased in the combination group (t=12. 36, 5. 99, 15. 47,P<0. 05). Compared with control group, the percentages of cells in G2/M phase were all significantly increased in apatinib group, radiation group and combination group (t=8. 81, 39. 69, 20. 61,P<0. 05). Compared with radiation alone group and control group, the percentage of cells in S phase significantly increased in apatinib alone group and combination group(t = 6.06, 3.82,8.81,6.24,P < 0.05). Conclusions Apatinib can increase radiosensitivity of esophageal cancer cell line Kyse-150 possibly by inhibiting cell proliferation, inducing cell apoptosis and causing redistribution of cell cycle.
Texto completo:
Disponível
Base de dados:
WPRIM (Pacífico Ocidental)
Idioma:
Chinês
Revista:
Chinese Journal of Radiological Medicine and Protection
Ano de publicação:
2017
Tipo de documento:
Artigo