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在去势抵抗性前列腺癌中，曲林通过上调miR-145-5p抑制MAP3K11/NF-κB/COX-2信号通路。

Trillin inhibits MAP3K11/NF-κB/COX-2 signaling pathways through upregulation of miR-145-5p in castration-resistant prostate cancer.

作者信息

Wang Yanlong, Peng Yulin, Hao Wenjun, He Chengjian, Gao Xiang, Liang Peng, Zhao Haolin, Wang Ying, Wang Liang, Yu Zhenlong, Liu Zhiyu

机构信息

Department of Urology, The Second Hospital of Dalian Medical University, Dalian 116023, China.

College of Integrative Medicine, College of Pharmacy, Dalian Medical University, Dalian 116044, China.

出版信息

iScience. 2024 Dec 2;28(2):111505. doi: 10.1016/j.isci.2024.111505. eCollection 2025 Feb 21.

DOI:10.1016/j.isci.2024.111505
PMID:39898047
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11787546/
Abstract

Castration-resistant prostate cancer (CRPC) presents a significant challenge in treatment following androgen deprivation therapy. This study evaluates Trillin, a compound with antioxidant and anti-inflammatory properties, for its therapeutic potential against CRPC. Using DU145 and PC3 cell lines and a mouse xenograft model, we demonstrate that Trillin effectively inhibits CRPC cell viability, proliferation, migration, and invasion while promoting apoptosis and cell-cycle arrest. Mechanistic investigations reveal that Trillin disrupts NF-κB/COX-2 signaling by downregulating MAP3K11 and COX-2 and inhibiting the nuclear translocation of NF-κB subunits. Additionally, Trillin enhances the expression of miR-145-5p, further modulating pathways critical for CRPC progression. These findings suggest that Trillin may offer a promising alternative approach for targeting CRPC, highlighting its potential as a therapeutic agent to improve patient outcomes.

摘要

去势抵抗性前列腺癌（CRPC）在雄激素剥夺治疗后的治疗中构成了重大挑战。本研究评估了具有抗氧化和抗炎特性的化合物曲菌素（Trillin）对CRPC的治疗潜力。使用DU145和PC3细胞系以及小鼠异种移植模型，我们证明曲菌素可有效抑制CRPC细胞的活力、增殖、迁移和侵袭，同时促进细胞凋亡和细胞周期停滞。机制研究表明，曲菌素通过下调MAP3K11和COX-2并抑制NF-κB亚基的核转位来破坏NF-κB/COX-2信号通路。此外，曲菌素增强了miR-145-5p的表达，进一步调节了对CRPC进展至关重要的信号通路。这些发现表明，曲菌素可能为靶向治疗CRPC提供一种有前景的替代方法，突出了其作为改善患者预后的治疗药物的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca92/11787546/ae7d4b4a2cbd/gr11.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca92/11787546/9c64f71caf0a/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca92/11787546/5fa7df7362c4/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca92/11787546/ccbad77f95b7/gr2.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca92/11787546/4c51443fc9e2/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca92/11787546/25d32b015282/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca92/11787546/439e7a8a1f1d/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca92/11787546/ef822546dfbe/gr9.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca92/11787546/ae7d4b4a2cbd/gr11.jpg

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