[1]王源源,印学晨,董云菲,等.靶向碱基切除修复途径以克服结直肠癌细胞中的阿霉素耐药性[J].南京师大学报(自然科学版),2023,46(02):61-69.[doi:10.3969/j.issn.1001-4616.2023.02.008]
　Wang Yuanyuan,Yin Xuechen,Dong Yunfei,et al.Targeting Base Excision Repair Pathway to Overcome Doxorubicin Resistance in Colorectal Cancer Cells[J].Journal of Nanjing Normal University(Natural Science Edition),2023,46(02):61-69.[doi:10.3969/j.issn.1001-4616.2023.02.008]
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靶向碱基切除修复途径以克服结直肠癌细胞中的阿霉素耐药性()
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《南京师大学报（自然科学版）》[ISSN:1001-4616/CN:32-1239/N]

卷:
第46卷
期数:
2023年02期
页码:
61-69
栏目:
生物学
出版日期:
2023-06-15

文章信息/Info

Title:
Targeting Base Excision Repair Pathway to Overcome Doxorubicin Resistance in Colorectal Cancer Cells
文章编号:
1001-4616(2023)02-0061-09
作者:
王源源; 印学晨; 董云菲; 刘 洁; 郭志刚; 何凌峰
(南京师范大学生命科学学院,江苏省分子与医学生物技术重点实验室,江苏 南京 210023)
Author(s):
Wang Yuanyuan; Yin Xuechen; Dong Yunfei; Liu Jie; Guo Zhigang; He Lingfeng
(School of Life Sciences,Nanjing Normal University,Jiangsu Key Laboratory for Molecular and Medical Biotechnology,Nanjing 210023,China)
关键词:
DNA修复; FEN1; 阿霉素; 结直肠癌; 肿瘤治疗
Keywords:
DNA repair;  FEN1;  Doxorubicin;  colorectal cancer cells;  tumor therapy
分类号:
R73-36+1
DOI:
10.3969/j.issn.1001-4616.2023.02.008
文献标志码:
A
摘要:
结直肠癌(CRC)具有非常高的发病率和死亡率,成为全球第三大最常见的恶性肿瘤和第二大最致命的癌症. 阿霉素作为化学治疗药物,多年来一直广泛应用于癌症临床治疗,但由于其耐药性和副作用,治疗效果较为有限. 已有研究证明,在癌细胞中DNA修复能力会大大增强,这在很大程度上会使得癌细胞在化学治疗药物引起的DNA损伤中存活下来. Flap核酸内切酶1(FEN1)在各种类型的癌细胞中表达较高,并在DNA损伤修复中起着关键作用. 研究表明,FEN1抑制剂SC13显著增强了阿霉素的治疗效果,这种联合治疗可以通过激活cyclinD-CDK4-6/INK4/Rb通路进而抑制结直肠癌的细胞增殖,故靶向FEN1可为阿霉素在临床使用中提供一种新的策略.
Abstract:
Colorectal cancer(CRC)has very high morbidity and mortality, becoming the third most common malignancy and the second most deadly cancer worldwide. As a chemotherapeutic drug, doxorubicin has been widely used in clinical treatment for many years but the therapeutic efficacy is limited due to drug resistance and side effects. Studies have shown that DNA repair capacity is greatly enhanced in cancer cells, which to a large extent enables cancer cells to survive DNA damage induced by chemotherapeutic drugs. Flap endonuclease 1(FEN1)expression gets elevated in various types of cancer cells and plays a critical role in DNA damage repair. The study revealed that FEN1 inhibitor SC13 significantly enhanced the therapeutic effect of doxorubicin. The combinative treatment suppressed colorectal cancer cells proliferation via the activation of cylinD-CDK4-6/INK4/Rb pathway. It suggested that targeting FEN1 could be a potent strategy for tumor-targeting therapy.

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相似文献/References:

[1]周婷,高婷婷,孙洪芳,等.结构特异性核酸内切酶FEN1及其与肿瘤的关系[J].南京师大学报(自然科学版),2014,37(02):7.
　Zhou Ting,Gao Tingting,Sun Hongfang,et al.FEN1’s Functional Regulation and Its Link to Cancer[J].Journal of Nanjing Normal University(Natural Science Edition),2014,37(02):7.

备注/Memo

备注/Memo:
收稿日期:2022-09-29.
基金项目:国家自然科学基金项目(81872284).
通讯作者:何凌峰,博士,副教授,研究方向:DNA损伤修复. E-mail:lfhe22@139.com
更新日期/Last Update: 2023-06-15