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松萝酸靶向14-3-3蛋白并通过阻断底物相互作用抑制癌症进展。

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

作者信息

Varlı Mücahit, Bhosle Suresh R, Kim Eunae, Yang Yi, Taş İsa, Zhou Rui, Pulat Sultan, Gamage Chathurika D B, Park So-Yeon, Ha Hyung-Ho, Kim Hangun

机构信息

College of Pharmacy, Sunchon National University, 255 Jungang-ro, Sunchon, Jeonnam 57922, Republic of Korea.

College of Pharmacy, Chosun University, 146 Chosundae-gil, Gwangju 61452, Republic of Korea.

出版信息

JACS Au. 2024 Apr 11;4(4):1521-1537. doi: 10.1021/jacsau.3c00774. eCollection 2024 Apr 22.

DOI:10.1021/jacsau.3c00774
PMID:38665668
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11040559/
Abstract

The anticancer therapeutic effects of usnic acid (UA), a lichen secondary metabolite, have been demonstrated and . 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.

摘要

地衣次生代谢产物松萝酸（UA）的抗癌治疗效果已得到证实。然而，UA抗癌作用的潜在机制仍有待阐明。在本研究中，使用UA-连接体-Affi-凝胶分子鉴定了UA的靶蛋白，结果表明UA与14-3-3蛋白结合。UA与14-3-3结合，导致蛋白酶体和自噬体蛋白降解。UA与14-3-3亚型的相互作用调节了结直肠癌中的细胞侵袭、细胞周期进程、有氧糖酵解、线粒体生物合成以及Akt/mTOR、JNK、STAT3、NF-κB和AP-1信号通路。14-3-3的肽抑制剂阻断或逆转了UA的活性并抑制了其作用。结果表明，UA与14-3-3亚型结合，并通过影响14-3-3靶标和磷酸化蛋白来抑制癌症进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc47/11040559/a9ff4d6308c2/au3c00774_0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc47/11040559/ad4939e00189/au3c00774_0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc47/11040559/f705f9dcae75/au3c00774_0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc47/11040559/fbc19f2c6161/au3c00774_0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc47/11040559/076fc07c881f/au3c00774_0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc47/11040559/2d1819f13abe/au3c00774_0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc47/11040559/b6354eb424bc/au3c00774_0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc47/11040559/a9ff4d6308c2/au3c00774_0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc47/11040559/ad4939e00189/au3c00774_0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc47/11040559/f705f9dcae75/au3c00774_0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc47/11040559/fbc19f2c6161/au3c00774_0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc47/11040559/076fc07c881f/au3c00774_0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc47/11040559/2d1819f13abe/au3c00774_0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc47/11040559/b6354eb424bc/au3c00774_0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc47/11040559/a9ff4d6308c2/au3c00774_0007.jpg

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