| 于大海,周冲,田野.复制蛋白A在食管癌细胞株辐射抗性中的作用及其机制[J].中华放射医学与防护杂志,2012,32(4):347-349,368.YU Da-hai,ZHOU Chong,TIAN Ye.Role of replication protein A in the radioresistance of esophageal cancer cell line and its mechanism[J].Chin J Radiol Med Prot,2012,32(4):347-349,368 |
| 复制蛋白A在食管癌细胞株辐射抗性中的作用及其机制 |
| Role of replication protein A in the radioresistance of esophageal cancer cell line and its mechanism |
| 投稿时间：2012-03-25 |
| DOI：10.3760/cma.j.issn.0254-5098.2012.04.003 |
| 中文关键词: 复制蛋白A 放射敏感性 食管癌细胞 |
| 英文关键词:Replication protein A Radiosensitivity Esophageal cancer cell |
| 基金项目:徐州市科技局资助项目(XM08C057) |
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| 中文摘要: |
| 目的 研究抑制复制蛋白A(RPA)基因表达对辐射抗性食管癌细胞株TE-1R辐射敏感性的影响,并探讨其潜在的作用机制。方法 以TE-1为亲代构建辐射抗性模型TE-1R细胞株,通过siRNA敲低TE-1R细胞株RPA1和RPA2基因表达,并以未转染(Con)组和无意序列(NC)组作对照,应用克隆形成实验绘制细胞存活曲线,采用流式细胞仪测定细胞周期,观察TE-1R细胞株的辐射敏感性变化。结果 siRNA转染48 h后,RPA1及RPA2蛋白表达较Con和NC组降低。与NC组比较,RPA1 siRNA转染组及RPA2 siRNA转染组细胞的D0、Dq、SF2值由2.09、1.70、0.85分别降至1.67、0.71、0.44及1.82、0.89、0.51,放射增敏比SERDq分别为2.39和1.91。抑制RPA1或RPA2表达后可观察到G2/M期阻滞现象,与NC组比较,G2/M期细胞比例由(18.70±3.14)%增至(26.95±3.96)%及(25.28±2.74)%(t=2.83、2.85,P<0.05)。结论 通过抑制RPA1或RPA2表达,可以提高辐射抗性食管癌细胞株TE-1R的辐射敏感性。其潜在的作用机制可能是改变细胞周期分布,减少了受照射细胞亚致死损伤的修复。 |
| 英文摘要: |
| Objective To evaluate the effect of replication protein A (RPA) gene suppression on the radiosensitivity of esophageal cancer cells (TE-1R) and underlying mechanism.Methods A radioresistant human esophageal cancer cell line TE-1R was screened out by fractionated irradiation to TE-1 cells, then siRPA1 or siRPA2 was transfected to TE-1R cells. The untransfected (Con) group and nonsense siRNA transfected (NC) group were set as control groups. The survival was measured with colony-forming assay and the cell cycle distribution was measured with flow cytometry. Results Compared with the Con and NC groups, the protein expression of RPA1 and RPA2 decreased significantly 48 h after siRPA1 and siRPA2 transfection. The D0, Dq, and SF2 values reduced from 2.09, 1.70, 0.85 in NC group to 1.67, 0.71, 0.44 and 1.82, 0.89, 0.51 in siRPA1 and siRPA2 transfection groups, respectively. Accordingly, the sensitization enhancement ratios of Dq were 2.39 and 1.91, respectively. The G2/M arrest in siRPA1 and siRPA2 transfection groups increased from (18.70±3.14)% of NC group to (26.95±3.96)% and (25.28±2.74)% (t=2.827, 2.853, P<0.05), respectively. Conclusions Knocking down of RPA1 or RPA2 genes can enhance the raidosensitivity of human esophageal cancer cells TE-1R, where the inhibition of radiation-induced sublethal damage repair may be involved. Accordingly, RPA may become a new target of radiosensitization in esophageal cancer. |
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