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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.
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To study effects of 9 cis retinoic acid (9 cisRA) on biological characteristics of lung squamous cancer cells, cell growth, cell differentiation and apoptotic indexes were observed in 9 cisRA treated L 78 and A 2 lung squamous cancer cells with flow cytometry. The results showed that 9 cisRA exerted marked inhibitory effect on the growth of two lung squamous cancer cell lines, 9 cisRA also had significant inducing effect on the differentiation of L 78 and A 2 cell lines, whereas the percentages of apoptosis of two cell lines in the treatment group were significantly higher than the control group. We conclude that 9 cisRA could inhibit growth inhibition, induce cell differentiation and apoptosis of L 78 and A 2 lung squamous cancer cells