BRCA2 affects the efficiency of DNA double-strand break repair in response to N-nitroso compounds with differing carcinogenic potentials
文献类型：期刊论文
| 作者 | Zhao, Wen-Ting; Wang, Yu-Tian; Huang, Zhao-Wei; Fang, Jing（方靖） |
| 刊名 | ONCOLOGY LETTERS
 |
| 出版日期 | 2013 |
| 卷号 | 5期号:6页码:1948-1954 |
| 关键词 | DNA double strand breaks BRCA2 N-nitroso compounds DNA damage repair |
| 通讯作者 | Wang, YT (reprint author), Second Mil Med Univ, Changzheng Hosp, Dept Gastroenterol, 415 Fengyang Rd, Shanghai 200031, Peoples R China. |
| 英文摘要 | The tumor suppressor gene breast cancer susceptibility gene 2 (BRCA2) is frequently mutated or epigenetically repressed in human cancer and has a significant role in the homologous recombination (HR) of DNA double-strand breaks (DSBs). Although N-nitrosodiethylamine (NDEA), N-nitrosodiethanolamine (NDELA) and N-nitrosodipropylamine (NDPA) have similar chemical structures and are able to induce DNA damage, they have varying carcinogenic risks. We hypothesized that the DNA damage repair pathways that are induced by these N-nitroso compounds (NOCs) may differ and that this may contribute to the genotoxic-carcinogenic effect of the NOCs. The present study aimed to characterize the formation of DSBs by NDEA, NDELA and NDPA and also to investigate whether BRCA2 is involved in the DNA damage response. The NOCs were observed to time-dependently induce DSBs and the expression of gamma-H2AX in gastric cancer SGC7901 cells. It was observed that the DNA damage induced by NDEA, the most potent carcinogen, was not repaired as efficiently as that caused by NDELA or NDPA. The expression of BRCA2 and RAD51 was demonstrated to be inhibited by NDEA treatment but upregulated by NDELA or NDPA treatment. Furthermore, the knock down of BRCA2 expression impaired the DNA damage repair induced by NDELA or NDPA. The cells with this knock down exhibited an increased sensitivity to NDELA or NDPA treatment, but not to NDEA. These findings suggest that a BRCA2-mediated pathway contributes to differential DSB repair and sensitivity in response to NOC exposure and that it may be associated with the genotoxic-carcinogenic potential of NOCs. |
| 类目[WOS] | Oncology |
| 研究领域[WOS] | Oncology |
| 关键词[WOS] | CANCER SUSCEPTIBILITY ; H2A PHOSPHORYLATION ; CELLULAR-RESPONSE ; ANTICANCER AGENT ; IN-VIVO ; RECOMBINATION ; GENE ; CHEMORESISTANCE ; MUTATIONS ; NITROSAMINES |
| 收录类别 | SCI |
| 语种 | 英语 |
| WOS记录号 | WOS:000324816500038 |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.144/handle/331004/335]  |
| 专题 | 中国科学院上海生命科学研究院营养科学研究所_营养与癌症研究组 |
| 推荐引用方式 GB/T 7714 | Zhao, Wen-Ting,Wang, Yu-Tian,Huang, Zhao-Wei,et al. BRCA2 affects the efficiency of DNA double-strand break repair in response to N-nitroso compounds with differing carcinogenic potentials[J]. ONCOLOGY LETTERS,2013,5(6):1948-1954. |
| APA | Zhao, Wen-Ting,Wang, Yu-Tian,Huang, Zhao-Wei,&Fang, Jing.(2013).BRCA2 affects the efficiency of DNA double-strand break repair in response to N-nitroso compounds with differing carcinogenic potentials.ONCOLOGY LETTERS,5(6),1948-1954. |
| MLA | Zhao, Wen-Ting,et al."BRCA2 affects the efficiency of DNA double-strand break repair in response to N-nitroso compounds with differing carcinogenic potentials".ONCOLOGY LETTERS 5.6(2013):1948-1954. |
入库方式： OAI收割
来源：上海营养与健康研究所
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