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作 者:毕建平[1] 马虹[1] 张涛[1] 张盛[1] 李勤[1]
机构地区:[1]华中科技大学同济医学院附属协和医院肿瘤中心,武汉430023
出 处:《华中科技大学学报(医学版)》2014年第2期148-152,157,共6页Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基 金:吴阶平基金资助项目(No.320.6750.1259)
摘 要:目的研究盐酸埃克替尼联合放疗抗肿瘤的效果及机制。方法建立裸鼠人大肠腺癌HT29细胞株荷瘤模型,随机分为4组:对照组、盐酸埃克替尼组、放疗组、联合治疗组,用免疫荧光方法检测肿瘤组织γ-H2AX、53BP1表达,及细胞增殖相关抗原Ki-67和凋亡相关抗原Caspase-3的表达,并计算组织细胞内γ-H2AX、53BP1荧光焦点平均值以及肿瘤增殖率和肿瘤凋亡数。结果盐酸埃克替尼联合放疗组较其他3组显著增加肿瘤组织γ-H2AX和53BP1的表达,抑制肿瘤细胞增殖(Ki-67阳性细胞率降低)和增加肿瘤细胞凋亡(Caspase-3阳性细胞数增加)(均P<0.01)。结论盐酸埃克替尼与放疗同步显著加重肿瘤细胞内的DNA损伤,抑制肿瘤增殖,增加肿瘤凋亡,从而增进放疗疗效。Objective To examine the antitumor efficacy of a combination of icotinib hydrochloride and radiotherapy in a human tumor xenograft model.Methods Tumor-bearing nude mouse models were established by using HT29cells(a human colorectal adenocarcinoma cell line).Four groups were set up in terms of different treatments(administration of icotinib hydrochloride or irradiation):control group,icotinib hydrochloride group;radiotherapy(RT)group;icotinib hydrochloride+RT group.The expressions ofγ-H2AX,53BP1Ki-67and Caspase-3were detected by immunofluorescence.The average fluorescent values ofγ-H2AX and 53BP1were obtained,and the proliferation rate of tumor cells and the number of apoptotic cells calculated.Results Icotinib hydrochloride combined with RT significantly inhibited the DNA repair by increasing the expression ofγ-H2AX and 53BP1and the treatment could inhibit the proliferation and increase the apoptosis of tumor tissue(P〈0.01). Conclusion Icotinib hydrochloride combined with RT enhances the radiosensitivity of tumor cells by aggravating the DNA injury,inhibiting the proliferation and increasing apoptosis of tumor cells.
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