YOU Zhen-yu,ZHAO Yong,JIANG Ping,et al.Mechanism of radiosensitizing effects of endostatin on H-520 human lung squamous cancer cells[J].Chinese Journal of Radiological Medicine and Protection,2010,30(3):287-290
Mechanism of radiosensitizing effects of endostatin on H-520 human lung squamous cancer cells
Received:July 13, 2009  
DOI:10.3760/cma.j.issn.0254-5098.2010.03.015
KeyWords:Endostatin  Lung squamous cancer  Radiosensitization  p38-MAPK  Akt
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Author NameAffiliationE-mail
YOU Zhen-yu Cancer Center, Peking University Third Hospital, Beijing 100191, China  
ZHAO Yong 中国科学院动物研究所生物膜与膜生物工程国家重点实验室  
JIANG Ping Cancer Center, Peking University Third Hospital, Beijing 100191, China  
MENG Na Cancer Center, Peking University Third Hospital, Beijing 100191, China  
WANG Jun-jie Cancer Center, Peking University Third Hospital, Beijing 100191, China doctorjunjiewang@yahoo.com.cn 
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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 levels 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/G1arrest, cell apoptosis and down-regulation of gene expression of cyclin D1, cdk2, cdk4 and reduces the phosphorylation of Akt and p38-MAPK.
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