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金诺芬,一种抗风湿药物,通过抑制Stat3信号显示出抗癌干细胞的潜力。

Auranofin, an antirheumatic drug, shows anticancer stem cell potential via suppression of the Stat3 signal.

作者信息

Ko Seung-Yeon, Kim Yuna, Chung Jin Sun, Kim Young Bin, Kim Su-Lim, Lee Dong-Sun, Chun Kyung-Hee, Choi Hack Sun

机构信息

Department of Biochemistry & Molecular Biology, Graduate School of Medical Science, Brain Korea 21 Project, Yonsei University College of Medicine, Seoul 03722, Korea.

Faculty of Biotechnology, College of Applied Life Sciences, Jeju National University, SARI, Jeju 63243, Korea.

出版信息

BMB Rep. 2025 Jul;58(7):293-299.

Abstract

Accumulating data have shown that targeting breast cancer stem cells (CSCs) is an auspicious way for anticancer therapies. This study demonstrated that the antirheumatic drug auranofin is a potent CSC inhibitor with anti-CSC action on breast cancer. This research focused on investigating the effect of auranofin on breast cancer and CSCs and its cellular mechanism. Mammosphere formation, colony formation, levels of CD44high/CD24low, and aldehyde dehydrogenase 1 expression in the cells were evaluated after auranofin treatment. The anti-CSC properties of auranofin were further examined by gel shift assay and cytokine detection. Auranofin suppressed cell growth, colony formation, migration, and mammosphere formation and triggered apoptosis in breast cancer. Auranofin decreased the CD44high/CD24low- and aldehyde dehydrogenaseexpressed subpopulations, as well as the Stat3-DNA interaction and phosphorylated Stat3 level. Auranofin also decreased the extracellular levels of interleukin-8 (IL-8) in the mammosphere media. Auranofin suppressed the Stat3/IL-8 signal and killed CSCs; therefore, it may be a potential target for CSCs. [BMB Reports 2025; 58(7): 293-299].

摘要

越来越多的数据表明,靶向乳腺癌干细胞(CSCs)是一种有前景的抗癌治疗方法。本研究表明,抗风湿药物金诺芬是一种有效的CSC抑制剂,对乳腺癌具有抗CSC作用。本研究聚焦于探究金诺芬对乳腺癌和CSCs的影响及其细胞机制。在金诺芬处理后,评估细胞中的乳腺球形成、集落形成、CD44高/CD24低水平以及醛脱氢酶1的表达。通过凝胶迁移试验和细胞因子检测进一步研究金诺芬的抗CSC特性。金诺芬抑制乳腺癌细胞的生长、集落形成、迁移和乳腺球形成,并引发细胞凋亡。金诺芬降低了CD44高/CD24低和醛脱氢酶表达的亚群,以及Stat3与DNA的相互作用和磷酸化Stat3水平。金诺芬还降低了乳腺球培养基中白细胞介素-8(IL-8)的细胞外水平。金诺芬抑制Stat3/IL-8信号并杀死CSCs;因此,它可能是CSCs的一个潜在靶点。[《BMB报告》2025年;58(7): 293 - 299]

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