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Usnic Acid Targets 14-3-3 Proteins and Suppresses Cancer Progression by Blocking Substrate Interaction

Varlı, Mücahit ; Bhosle, Suresh R ; Kim, Eunae ; Yang, Yi ; Taş, İsa LU orcid ; Zhou, Rui ; Pulat, Sultan ; Gamage, Chathurika D B ; Park, So-Yeon and Ha, Hyung-Ho , et al. (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.

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publishing date
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}},
}