Cordycepin generally inhibits growth factor signal transduction in a systems pharmacology study.

IF 3.5 4区 生物学 Q1 Biochemistry, Genetics and Molecular Biology FEBS Letters Pub Date : 2024-11-07 DOI:10.1002/1873-3468.15046
Steven Lawrence, Jialiang Lin, Asma Khurshid, Wahyu Utami, Richa Singhania, Sadaf Ashraf, Graeme J Thorn, Irengbam Rocky Mangangcha, Keith Spriggs, Dong-Hyun Kim, David Barrett, Cornelia H de Moor
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Abstract

Cordycepin (3' deoxyadenosine) has been widely researched as a potential cancer therapy, but many diverse mechanisms of action have been proposed. Here, we confirm that cordycepin triphosphate is likely to be the active metabolite of cordycepin and that it consistently represses growth factor-induced gene expression. Bioinformatic analysis, quantitative PCR and western blotting confirmed that cordycepin blocks the PI3K/AKT/mTOR and/or MEK/ERK pathways in six cell lines and that AMPK activation is not required. The effects of cordycepin on translation through mTOR pathway repression were detectable within 30 min, indicating a rapid process. These data therefore indicate that cordycepin has a universal mechanism of action, acting as cordycepin triphosphate on an as yet unknown target molecule involved in growth factor signalling.

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在一项系统药理学研究中,虫草素通常会抑制生长因子信号转导。
虫草素(3'脱氧腺苷)作为一种潜在的癌症疗法已被广泛研究,但人们提出了许多不同的作用机制。在这里,我们证实虫草素三磷酸酯可能是虫草素的活性代谢产物,而且它能持续抑制生长因子诱导的基因表达。生物信息学分析、定量 PCR 和 Western 印迹证实,虫草素在六种细胞系中阻断了 PI3K/AKT/mTOR 和/或 MEK/ERK 通路,而不需要激活 AMPK。通过抑制 mTOR 通路,虫草素对翻译的影响在 30 分钟内就能被检测到,表明这是一个快速的过程。因此,这些数据表明,虫草素具有一种普遍的作用机制,它以三磷酸虫草素的形式作用于参与生长因子信号传导的未知靶分子。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
FEBS Letters
FEBS Letters 生物-生化与分子生物学
CiteScore
7.00
自引率
2.90%
发文量
303
审稿时长
1.0 months
期刊介绍: FEBS Letters is one of the world''s leading journals in molecular biology and is renowned both for its quality of content and speed of production. Bringing together the most important developments in the molecular biosciences, FEBS Letters provides an international forum for Minireviews, Research Letters and Hypotheses that merit urgent publication.
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