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一种新型抗癌药物乙酰丹参酮 IIA 通过下调雌激素受体抑制雌激素受体阳性乳腺癌细胞生长。

A novel anti-cancer agent, acetyltanshinone IIA, inhibits oestrogen receptor positive breast cancer cell growth by down-regulating the oestrogen receptor.

机构信息

Division of Bioengineering, School of Chemical and Biomedical Engineering, Nanyang Technological University, Singapore.

School of Biological Sciences, Nanyang Technological University, Singapore.

出版信息

Cancer Lett. 2014 Apr 28;346(1):94-103. doi: 10.1016/j.canlet.2013.12.023. Epub 2013 Dec 24.

Abstract

In this paper we show that acetyltanshinone IIA (ATA), a novel anti-cancer agent, preferentially inhibits cell growth of oestrogen receptor positive (ER+) breast cancer cells and that it is more potent than the commonly used anti-breast cancer agent, tamoxifen. The metabolic product of ATA, hydroquinone tanshinone IIA (HTA) binds to the ERα and causes its degradation mainly in the nucleus via an ubiquitin-mediated proteasome-dependent pathway. In addition, ATA also reduced the mRNA levels of the ERα encoding gene, ESR1, distinguishing ATA from another anti-breast cancer drug, fulvestrant. Finally, ATA reduced the transcription of an ER-responsive gene, GREB1.

摘要

在本文中,我们证明了新型抗癌药物乙酰丹参酮 IIA(ATA)优先抑制雌激素受体阳性(ER+)乳腺癌细胞的生长,其效力强于常用的乳腺癌治疗药物他莫昔芬。ATA 的代谢产物对苯二酚丹参酮 IIA(HTA)与 ERα 结合,并通过泛素介导的蛋白酶体依赖性途径主要在核内导致其降解。此外,ATA 还降低了 ERα 编码基因 ESR1 的 mRNA 水平,这使 ATA 有别于另一种乳腺癌药物氟维司群。最后,ATA 降低了 ER 反应性基因 GREB1 的转录。

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