FEN1抑制剂SC13逆转MCF-7/ADR细胞的耐药性研究  

FEN1 Inhibitor SC13 Reverses the Drug Resistance of MCF-7/ADR Cells

作　　者：刘洁 王源源 郭志刚 何凌峰 Liu Jie;Wang Yuanyuan;Guo Zhigang;He Lingfeng(School of Life Sciences,Nanjing Normal University,Jiangsu Key Laboratory for Molecular and Medical Biotechnology,Nanjing 210023,China)

机构地区：[1]南京师范大学生命科学学院,江苏分子与医学生物技术重点实验室,江苏南京210023

出　　处：《南京师大学报（自然科学版）》2024年第4期77-85,共9页Journal of Nanjing Normal University(Natural Science Edition)

基　　金：国家自然科学基金项目(81872284)。

摘　　要：癌细胞在化疗过程中产生的多药耐药性(multidrug resistance,MDR)仍然是目前临床治疗乳腺癌所面临的巨大挑战.肿瘤细胞中强大的DNA损伤修复能力可能是导致其耐药性的主要原因之一.研究发现,碱基切除修复(base excision repair,BER)途径中的关键蛋白Flap核酸内切酶1(FEN1)在耐阿霉素的人乳腺癌细胞(MCF-7/ADR)中高表达,并且FEN1抑制剂SC13可以显著增强阿霉素对于MCF-7/ADR的治疗敏感性,其具体的作用机制可能是通过cGAS-STING-NFκB信号通路激活了抗肿瘤免疫反应.The development of multidrug resistance(MDR)in cancer cells during chemotherapy poses a significant challenge in the clinical treatment of breast cancer.One of the main contributors to drug resistance is the robust DNA damage repair capability of tumor cells.The research had revealed that Flap endonuclease 1(FEN1),a core protein involved in the base excision repair(BER)pathway,was highly expressed in adriamycin-resistant breast cancer cells.Moreover,the study found that the FEN1 inhibitor SC13 significantly enhanced the sensitivity of MCF-7/ADR cells to adriamycin.While the precise mechanism of action was not yet fully understood,it was hypothesized that the enhanced sensitivity of MCF-7/ADR cells may be attributed to the activation of potent antitumor responses mediated by the cGAS-STING-NFκB signaling pathways.

关 键 词：乳腺癌 Flap核酸内切酶1 阿霉素 肿瘤治疗 化疗耐药 

分 类 号：R3[医药卫生—基础医学] F36[经济管理—产业经济]