Usnic Acid Targets 14-3-3 Proteins and Suppresses Cancer Progression by Blocking Substrate Interaction
(2024) In JACS Au 4(4). p.1521-1537- Abstract
The anticancer therapeutic effects of usnic acid (UA), a lichen secondary metabolite, have been demonstrated in vitro and in vivo. However, the mechanism underlying the anticancer effect of UA remains to be clarified. In this study, the target protein of UA was identified using a UA-linker-Affi-Gel molecule, which showed that UA binds to the 14-3-3 protein. UA binds to 14-3-3, causing the degradation of proteasomal and autophagosomal proteins. The interaction of UA with 14-3-3 isoforms modulated cell invasion, cell cycle progression, aerobic glycolysis, mitochondrial biogenesis, and the Akt/mTOR, JNK, STAT3, NF-κB, and AP-1 signaling pathways in colorectal cancer. A peptide inhibitor of 14-3-3 blocked or regressed the activity of UA and... (More)
The anticancer therapeutic effects of usnic acid (UA), a lichen secondary metabolite, have been demonstrated in vitro and in vivo. However, the mechanism underlying the anticancer effect of UA remains to be clarified. In this study, the target protein of UA was identified using a UA-linker-Affi-Gel molecule, which showed that UA binds to the 14-3-3 protein. UA binds to 14-3-3, causing the degradation of proteasomal and autophagosomal proteins. The interaction of UA with 14-3-3 isoforms modulated cell invasion, cell cycle progression, aerobic glycolysis, mitochondrial biogenesis, and the Akt/mTOR, JNK, STAT3, NF-κB, and AP-1 signaling pathways in colorectal cancer. A peptide inhibitor of 14-3-3 blocked or regressed the activity of UA and inhibited its effects. The results suggest that UA binds to 14-3-3 isoforms and suppresses cancer progression by affecting 14-3-3 targets and phosphorylated proteins.
(Less)
- author
- publishing date
- 2024-04-22
- type
- Contribution to journal
- publication status
- published
- subject
- in
- JACS Au
- volume
- 4
- issue
- 4
- pages
- 1521 - 1537
- publisher
- The American Chemical Society (ACS)
- external identifiers
-
- scopus:85190307241
- pmid:38665668
- ISSN
- 2691-3704
- DOI
- 10.1021/jacsau.3c00774
- language
- English
- LU publication?
- no
- additional info
- © 2024 The Authors. Published by American Chemical Society.
- id
- cbdd9a0b-3b07-4085-a863-bca7fbfd66d8
- date added to LUP
- 2026-09-23 15:56:08
- date last changed
- 2026-10-09 03:01:11
@article{cbdd9a0b-3b07-4085-a863-bca7fbfd66d8,
abstract = {{<p>The anticancer therapeutic effects of usnic acid (UA), a lichen secondary metabolite, have been demonstrated in vitro and in vivo. However, the mechanism underlying the anticancer effect of UA remains to be clarified. In this study, the target protein of UA was identified using a UA-linker-Affi-Gel molecule, which showed that UA binds to the 14-3-3 protein. UA binds to 14-3-3, causing the degradation of proteasomal and autophagosomal proteins. The interaction of UA with 14-3-3 isoforms modulated cell invasion, cell cycle progression, aerobic glycolysis, mitochondrial biogenesis, and the Akt/mTOR, JNK, STAT3, NF-κB, and AP-1 signaling pathways in colorectal cancer. A peptide inhibitor of 14-3-3 blocked or regressed the activity of UA and inhibited its effects. The results suggest that UA binds to 14-3-3 isoforms and suppresses cancer progression by affecting 14-3-3 targets and phosphorylated proteins.</p>}},
author = {{Varlı, Mücahit and Bhosle, Suresh R and Kim, Eunae and Yang, Yi and Taş, İsa and Zhou, Rui and Pulat, Sultan and Gamage, Chathurika D B and Park, So-Yeon and Ha, Hyung-Ho and Kim, Hangun}},
issn = {{2691-3704}},
language = {{eng}},
month = {{04}},
number = {{4}},
pages = {{1521--1537}},
publisher = {{The American Chemical Society (ACS)}},
series = {{JACS Au}},
title = {{Usnic Acid Targets 14-3-3 Proteins and Suppresses Cancer Progression by Blocking Substrate Interaction}},
url = {{http://dx.doi.org/10.1021/jacsau.3c00774}},
doi = {{10.1021/jacsau.3c00774}},
volume = {{4}},
year = {{2024}},
}
