FEN1 inhibitor(Nanyang Technological University)(FEN1 inhibitor(Nanyang Technological University)) - 药物靶点：FEN1_在研适应症：肿瘤_专利_临床

概要

基本信息

药物类型

小分子化药

别名-

靶点

FEN1

作用机制

FEN1 抑制剂(flap structure-specific endonuclease 1 inhibitors)

治疗领域

肿瘤

在研适应症

肿瘤

非在研适应症-

原研机构

Nanyang Technological University

在研机构

Nanyang Technological University

非在研机构-

最高研发阶段临床前

首次获批日期-

最高研发阶段(中国)-

特殊审评-

关联

100 项与 FEN1 inhibitor(Nanyang Technological University) 相关的临床结果

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100 项与 FEN1 inhibitor(Nanyang Technological University) 相关的转化医学

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100 项与 FEN1 inhibitor(Nanyang Technological University) 相关的专利（医药）

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1

项与 FEN1 inhibitor(Nanyang Technological University) 相关的文献（医药）

2024-01-01·International Journal of Biological Sciences

FOXA1-dependent PUS1 regulates EIF3b stability in a non-enzymatic pathway mediating prostate cancer bone metastasis

Article

作者: Guo, Zhenghui ; Zhong, Haitao ; Wu, Yongxin ; Peng, Shengmeng ; Huang, Hai ; Fu, Jianhan ; Cen, Meifeng ; Cheng, Bisheng ; Lai, Yiming ; Luo, Tianlong

Bone metastasis is a significant contributor to the poor prognosis in prostate cancer. Recent evidence highlights the pivotal role of pseudouridine synthases in solid tumor progression, yet the specific enzyme driving prostate cancer metastasis remains unidentified. This study uncovers a novel regulatory mechanism of the FOXA1/PUS1/EIF3b signaling axis in prostate cancer bone metastasis. We identified elevated PUS1 expression in prostate cancer tissues, correlating with higher clinical grade and worse prognosis. Knockdown of PUS1 inhibited metastasis independently of its enzymatic activity, with EIF3b acting as a downstream effector, protected from ubiquitin-mediated degradation by PUS1. Overexpression of EIF3b countered the metastasis suppression due to PUS1 knockdown. Additionally, FOXA1 was shown to enhance PUS1 expression by binding to its promoter. Mogroside IV-E, a specific PUS1 inhibitor, demonstrated potent anti-metastatic effects by reducing PUS1 expression. Our findings highlight the FOXA1/PUS1/EIF3b axis as a critical mediator of prostate cancer bone metastasis and suggest that targeting this pathway could be a promising therapeutic strategy.

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