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机构地区:[1]江苏大学附属医院呼吸科,江苏镇江212001
出 处:《南京医科大学学报(自然科学版)》2009年第11期1517-1520,共4页Journal of Nanjing Medical University(Natural Sciences)
摘 要:目的:研究X线对肺癌细胞X线修复交叉互补基因2((X-ray repair cross complementing gene2,XRCC2))与XRCC3表达水平的影响,探讨DNA同源重组修复机制在肺癌放疗过程中的作用。方法:以噻唑蓝还原法(MTT)检测X线对肺腺癌细胞株A549抑制率的影响,实时荧光定量RT-PCR技术检测X线处理肺癌细胞(人肺腺癌细胞株A549)后XRCC2和XRCC3mR-NA的表达水平。结果:肺癌细胞抑制率多数情况下随X线照射时间的延长及照射剂量的增大,细胞增殖抑制率增加,呈照射时间依赖性(P<0.05)和剂量依赖性(P<0.05),除了16Gy组与32Gy组比较无统计学意义(P=0.211)。X线照射后肺癌细胞XRCC2与XRCC3 mRNA的表达水平均先增高后降低,在照射后48h表达水平达高峰(P<0.05),且随着照射剂量的增大,XRCC2与XR-CC3 mRNA的表达水平也随之增加(P<0.05)。结论:X线照射可引起肺癌细胞XRCC2与XRCC3 mRNA表达水平的明显改变,表明DNA同源重组修复机制可能在肺癌放疗耐受中起了重要的作用。Objective:To study the effect of X-ray on expression levels of X-ray repair cross-complementing gene2(XRCC2)and XRCC3 in lung cancer cells, and explore the effect of DNA homologous recombination repair mechanism in radiotherapy of lung cancer. Methods: Cell inhibition ratio was measured using MTT assay. The expression levels of XRCC2 mRNA and XRCC3 mRNA in lung cancer cell line A549 were measured by RFQ-PCR assay. Results :The rate of proliferation inhibiting of lung cancer cells increased in line with the prolong radiation time of X-ray(P 〈 0.05)and the increase of radiation dose(P 〈 0.05),but there was no difference between the groups of 16 Gy and 32 Gy (P=0.211). The expression levels of XRCC2 and XRCC3 mRNA in these lung cancer cells increased significantly after treated with X-ray, and then decreased. The expression levels of XRCC2 and XRCC3 mRNA peaked at 48 h after X-ray treatment (P 〈 0.05). The expression levels of XRCC2 and XRCC3 mRNA increased markedly with the increase of radiation dose (P 〈 0.05). Conclusion:X-ray has a fairly obvious function to decrease proliferation of lung cancer cell, and could increase the expression levels of XRCC2 and XRCC3 mRNA in lung cancer cells. The results indicate that DNA homologous recombination repair mechanism may play an important role in resistance to radiotherapy in lung cancer cell.
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