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

Lawrence, Steven, Lin, Jialiang, Khurshid, Asma, Utami, Wahyu, Singhania, Richa, Ashraf, Sadaf, Thorn, Graeme, Mangangcha, Irengbam, Spriggs, Keith, Kim, Dong-Hyun, and others. (2025) Cordycepin generally inhibits growth factor signal transduction in a systems pharmacology study. FEBS Letters, 599 (3). pp. 415-435. ISSN 0014-5793. (doi:10.1002/1873-3468.15046) (KAR id:109968)

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Official URL: https://doi.org/10.1002/1873-3468.15046

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.

Item Type:	Article
DOI/Identification number:	10.1002/1873-3468.15046
Subjects:	R Medicine > RM Therapeutics. Pharmacology
Institutional Unit:	Schools > Medway School of Pharmacy
Former Institutional Unit:	There are no former institutional units.
Funders:	Versus Arthritis (https://ror.org/02jkpm469)
Depositing User:	Sadaf Ashraf
Date Deposited:	23 May 2025 14:54 UTC
Last Modified:	28 May 2025 02:41 UTC
Resource URI:	https://kar.kent.ac.uk/id/eprint/109968 (The current URI for this page, for reference purposes)

University of Kent Author Information

Ashraf, Sadaf.

Creator's ORCID:	https://orcid.org/0000-0001-5592-9122
CReDIT Contributor Roles:	Data curation, Writing - review and editing, Formal analysis, Investigation, Methodology

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