The radiosensitization effects of Endostar on human lung squamous cancer cells H-520

ES significantly inhibited H-520 cell proliferation in a time- and dose-dependent manner. According to the colony-forming assays, ES could increase the H-520 cell radiosensitivity. ES induced cell apoptosis, the apoptosis rate increased with the raise of ES concentration. Irradiation induced significantly higher apoptosis rate in ES-treated H-520 cells than non-treated H-520 cells. ES induced cell cycle distribution and G0/G1 arrest in H-520 cells, whereas irradiation induced G2/M arrest. The phospho-p38-MAPK and p-Akt protein levels were decreased in H-520 cells after ES treatment. Furthermore, activated caspase protein level increased and Bcl-2 protein levels decreased after treatment with ES and irradiation.ES significantly enhanced the sensitivity of H-520 cells to irradiation by inhibition of cellular proliferation, promotion of cell apoptosis and redistribution of cell cycle, possibly via deactivation of Akt pathway. The present study supports the possibility to use the combination of ES and ionizing irradiation to treat patients with lung squamous cell cancer in clinics.About 40% of patients with stage III or IV non-small cell lung carcinoma (NSCLC) cannot be resected at present [1]. Radiotherapy and chemotherapy are still the major treatment in such patients and significantly improves the survival of unresectable patients [1-3]. Nevertheless, long-term survival remains poor and mortality is high. Anti- angiogenesis therapy that interfered with cancer angiogenesis may improve lung cancer patient survival by enhancing radiation and chemotherapy efficiency without increasing treatment-related adverse effects [4-7].Endostatin (ED) is a 22 kDa polypeptide derived from the C-terminal fragment of type XVIII collogen. Both recombinant human and murine ED have been reported to inhibit endothelial cell proliferation but not smooth muscle cells or fibroblast proliferation in vitro, which suggested that the anti-proliferation effect was endothelial-specific [8,9]. The a