A Systematic Review of the Biological Effects of Cordycepin

Masar  Radhi; Sadaf Ashraf; Steven  Lawrence; Asta Arendt  Tranholm; Peter Arthur David  Wellham; Abdul  Hafeez; Ammar Sabah  Khamis; Robert  Thomas; Daniel  McWilliams; Cornelia  Huiberdina de Moor

doi:10.3390/molecules26195886

A Systematic Review of the Biological Effects of Cordycepin

Masar Radhi, Sadaf Ashraf, Steven Lawrence, Asta Arendt Tranholm, Peter Arthur David Wellham, Abdul Hafeez, Ammar Sabah Khamis, Robert Thomas, Daniel McWilliams, Cornelia Huiberdina de Moor ^* (Corresponding Author)

^*Corresponding author for this work

Research output: Contribution to journal › Review article › peer-review

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Abstract

We conducted a systematic review of the literature on the effects of cordycepin on cell survival and proliferation, inflammation, signal transduction and animal models. A total of 1204 publications on cordycepin were found by the cut-off date of 1 February 2021. After application of the exclusion criteria, 791 papers remained. These were read and data on the chosen subjects were extracted. We found 192 papers on the effects of cordycepin on cell survival and proliferation and calculated a median inhibitory concentration (IC50) of 135 µM. Cordycepin consistently repressed cell migration (26 papers) and cellular inflammation (53 papers). Evaluation of 76 papers on signal transduction indicated consistently reduced PI3K/mTOR/AKT and ERK signalling and activation of AMPK. In contrast, the effects of cordycepin on the p38 and Jun kinases were variable, as were the effects on cell cycle arrest (53 papers), suggesting these are cell-specific responses. The examination of 150 animal studies indicated that purified cordycepin has many potential therapeutic effects, including the reduction of tumour growth (37 papers), repression of pain and inflammation (9 papers), protecting brain function (11 papers), improvement of respiratory and cardiac conditions (8 and 19 papers) and amelioration of metabolic disorders (8 papers). Nearly all these data are consistent with cordycepin mediating its therapeutic effects through activating AMPK, inhibiting PI3K/mTOR/AKT and repressing the inflammatory response. We conclude that cordycepin has excellent potential as a lead for drug development, especially for age-related diseases. In addition, we discuss the remaining issues around the mechanism of action, toxicity and biodistribution of cordycepin.

Original language	English
Article number	5886
Number of pages	34
Journal	Molecules
Volume	26
Issue number	19
DOIs	https://doi.org/10.3390/molecules26195886
Publication status	Published - 28 Sept 2021

Bibliographical note

Funding: This work was supported by an award from the School of Pharmacy Research Committee (University of Nottingham) to Cornelia de Moor and Masar Radhi. Peter Wellham and Steven Lawrence were funded by the BBSRC DTP PhD programme [grant number BB/M008770/1]. Asta Tranholm was funded by a PhD studentship from Versus Arthritis awarded to Cornelia de Moor [grant number 21586].

Data Availability Statement

All data in the article were extracted from the cited papers as outlined in the Methods section.

Keywords

cordycepin
natural product
signal transduction
AKT
mTOR
AMPK
ERK
inflammation
cell viability
review

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Cite this

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abstract = "We conducted a systematic review of the literature on the effects of cordycepin on cell survival and proliferation, inflammation, signal transduction and animal models. A total of 1204 publications on cordycepin were found by the cut-off date of 1 February 2021. After application of the exclusion criteria, 791 papers remained. These were read and data on the chosen subjects were extracted. We found 192 papers on the effects of cordycepin on cell survival and proliferation and calculated a median inhibitory concentration (IC50) of 135 µM. Cordycepin consistently repressed cell migration (26 papers) and cellular inflammation (53 papers). Evaluation of 76 papers on signal transduction indicated consistently reduced PI3K/mTOR/AKT and ERK signalling and activation of AMPK. In contrast, the effects of cordycepin on the p38 and Jun kinases were variable, as were the effects on cell cycle arrest (53 papers), suggesting these are cell-specific responses. The examination of 150 animal studies indicated that purified cordycepin has many potential therapeutic effects, including the reduction of tumour growth (37 papers), repression of pain and inflammation (9 papers), protecting brain function (11 papers), improvement of respiratory and cardiac conditions (8 and 19 papers) and amelioration of metabolic disorders (8 papers). Nearly all these data are consistent with cordycepin mediating its therapeutic effects through activating AMPK, inhibiting PI3K/mTOR/AKT and repressing the inflammatory response. We conclude that cordycepin has excellent potential as a lead for drug development, especially for age-related diseases. In addition, we discuss the remaining issues around the mechanism of action, toxicity and biodistribution of cordycepin.",

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note = "Funding: This work was supported by an award from the School of Pharmacy Research Committee (University of Nottingham) to Cornelia de Moor and Masar Radhi. Peter Wellham and Steven Lawrence were funded by the BBSRC DTP PhD programme [grant number BB/M008770/1]. Asta Tranholm was funded by a PhD studentship from Versus Arthritis awarded to Cornelia de Moor [grant number 21586].",

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AU - Ashraf, Sadaf

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AU - Hafeez, Abdul

AU - Khamis, Ammar Sabah

AU - Thomas, Robert

AU - McWilliams, Daniel

AU - Huiberdina de Moor , Cornelia

N1 - Funding: This work was supported by an award from the School of Pharmacy Research Committee (University of Nottingham) to Cornelia de Moor and Masar Radhi. Peter Wellham and Steven Lawrence were funded by the BBSRC DTP PhD programme [grant number BB/M008770/1]. Asta Tranholm was funded by a PhD studentship from Versus Arthritis awarded to Cornelia de Moor [grant number 21586].

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N2 - We conducted a systematic review of the literature on the effects of cordycepin on cell survival and proliferation, inflammation, signal transduction and animal models. A total of 1204 publications on cordycepin were found by the cut-off date of 1 February 2021. After application of the exclusion criteria, 791 papers remained. These were read and data on the chosen subjects were extracted. We found 192 papers on the effects of cordycepin on cell survival and proliferation and calculated a median inhibitory concentration (IC50) of 135 µM. Cordycepin consistently repressed cell migration (26 papers) and cellular inflammation (53 papers). Evaluation of 76 papers on signal transduction indicated consistently reduced PI3K/mTOR/AKT and ERK signalling and activation of AMPK. In contrast, the effects of cordycepin on the p38 and Jun kinases were variable, as were the effects on cell cycle arrest (53 papers), suggesting these are cell-specific responses. The examination of 150 animal studies indicated that purified cordycepin has many potential therapeutic effects, including the reduction of tumour growth (37 papers), repression of pain and inflammation (9 papers), protecting brain function (11 papers), improvement of respiratory and cardiac conditions (8 and 19 papers) and amelioration of metabolic disorders (8 papers). Nearly all these data are consistent with cordycepin mediating its therapeutic effects through activating AMPK, inhibiting PI3K/mTOR/AKT and repressing the inflammatory response. We conclude that cordycepin has excellent potential as a lead for drug development, especially for age-related diseases. In addition, we discuss the remaining issues around the mechanism of action, toxicity and biodistribution of cordycepin.

AB - We conducted a systematic review of the literature on the effects of cordycepin on cell survival and proliferation, inflammation, signal transduction and animal models. A total of 1204 publications on cordycepin were found by the cut-off date of 1 February 2021. After application of the exclusion criteria, 791 papers remained. These were read and data on the chosen subjects were extracted. We found 192 papers on the effects of cordycepin on cell survival and proliferation and calculated a median inhibitory concentration (IC50) of 135 µM. Cordycepin consistently repressed cell migration (26 papers) and cellular inflammation (53 papers). Evaluation of 76 papers on signal transduction indicated consistently reduced PI3K/mTOR/AKT and ERK signalling and activation of AMPK. In contrast, the effects of cordycepin on the p38 and Jun kinases were variable, as were the effects on cell cycle arrest (53 papers), suggesting these are cell-specific responses. The examination of 150 animal studies indicated that purified cordycepin has many potential therapeutic effects, including the reduction of tumour growth (37 papers), repression of pain and inflammation (9 papers), protecting brain function (11 papers), improvement of respiratory and cardiac conditions (8 and 19 papers) and amelioration of metabolic disorders (8 papers). Nearly all these data are consistent with cordycepin mediating its therapeutic effects through activating AMPK, inhibiting PI3K/mTOR/AKT and repressing the inflammatory response. We conclude that cordycepin has excellent potential as a lead for drug development, especially for age-related diseases. In addition, we discuss the remaining issues around the mechanism of action, toxicity and biodistribution of cordycepin.

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KW - natural product

KW - signal transduction

KW - AKT

KW - mTOR

KW - AMPK

KW - ERK

KW - inflammation

KW - cell viability

KW - review

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U2 - 10.3390/molecules26195886

DO - 10.3390/molecules26195886

M3 - Review article

SN - 1420-3049

VL - 26

JO - Molecules

JF - Molecules

IS - 19

M1 - 5886

ER -

A Systematic Review of the Biological Effects of Cordycepin

Abstract

Bibliographical note

Data Availability Statement

Keywords

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