Mechanism of radiosensitizing effects of endostatin on H-520 human lung squamous cancer cells
10.3760/cma.j.issn.0254-5098.2010.03.015
- VernacularTitle:血管内皮抑素联合照射对肺癌H-520细胞周期及信号传导通路的影响
- Author:
Zhenyu YOU
;
Yong ZHAO
;
Ping JIANG
;
Na MENG
;
Junjie WANG
- Publication Type:Journal Article
- Keywords:
Endostatin;
Lung squamous cancer;
Radiosensitization;
p38-MAPK;
Akt
- From:
Chinese Journal of Radiological Medicine and Protection
2010;30(3):287-290
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the mechanism of radiosensitizing effects of endostatin on H-520 human lung squamous cancer cells.Methods H-520 cells was treated with endostatin and/or radiation.Colony-forming assays were used to indicate the radiosensitising effects.Cell cycle distribution and expression of phosphor-p38-MAPK were assayed by FCM,and cyclin D1,cdk2,cdk4 and survivin mRNA leveh were assayed by RT-PCR.Phosphor-Akt was evaluated by Western-blotting.Results Combination of endostatin and irradiation inhibited the proliferation of H-520 cells.According to the colony-forming assays,the D0,Dq,D10 and SF2 values of the combination groups were much lower than those of irradiation groups.The sensitization enhancement ratio(SER)was 1.51.G2/M arrest occurred after 4 Gy irradiation.The gene expression of cyclin D1,cdk2,ckd4 and survivin and phosphor-Akt protein were down-regulated after treatment.The expression of phosphor-p38-MAPK protein was also down-regulated after treatment with 200 μg/ml endostar.Conclusions Endostatin inhibits the growth of H-520 cells and radiosensitizes the cells by induction of G0/G1 arrest,cell apoptosis and down-regulation of gene expression of cyelin D1,cdk2,cdk4 and reduces the phosphorylation of Akt and p38-MAPK.
