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 |
FundProject: |
Author Name | Affiliation | E-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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