FKBP10 Promotes the Muscle Invasion of Bladder Cancer via Lamin A Dysregulation.

IF 8.2 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Xupeng Zhao, Jichen Wang, Shuo Tian, Lu Tang, Shouqing Cao, Jiali Ye, Tianwei Cai, Yundong Xuan, Xu Zhang, Xiubin Li, Hongzhao Li
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引用次数: 0

Abstract

Bladder cancer (BC) is a prevalent urinary malignancy and muscle-invasive bladder cancer (MIBC) is particularly aggressive and associated with poor prognosis. One of MIBC features is the nuclear atypia. However, the molecular mechanism underlying MIBC remains unclear. Here, we find that FKBP10 is significantly upregulated in MIBC tissues and correlated with metastasis and poor outcomes. FKBP10 promotes tumor cell invasion, migration, and metastasis, but not proliferation. Notably, FKBP10 enhances the nuclear atypia of BC cells. Mechanistically, FKBP10 interacts with prelamin A and hinder the nuclear entry of prelamin A, thereby leading to the decrease in the nuclear lamin A, a key factor involved in nuclear atypia. In human BC tissues, nuclear lamin A is downregulated and negatively correlated with FKBP10 expression. Overall, our findings demonstrate that the FKBP10/prelamin A/lamin A axis contributes to MIBC.

FKBP10通过层粘连蛋白A失调促进膀胱癌的肌肉侵袭。
膀胱癌(BC)是一种常见的泌尿系统恶性肿瘤,而肌肉浸润性膀胱癌(MIBC)侵袭性特别强,预后差。MIBC的特征之一是核非典型性。然而,MIBC的分子机制尚不清楚。在这里,我们发现FKBP10在MIBC组织中显著上调,并与转移和不良预后相关。FKBP10促进肿瘤细胞侵袭、迁移和转移,但不促进增殖。值得注意的是,FKBP10增强了BC细胞的核异型性。机制上,FKBP10与前纤层蛋白A相互作用,阻碍前纤层蛋白A进入细胞核,从而导致核纤层蛋白A减少,这是核非典型性的关键因素。在人BC组织中,核层粘连蛋白A与FKBP10表达下调并呈负相关。总之,我们的研究结果表明FKBP10/prelamin A/lamin A轴与MIBC有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
International Journal of Biological Sciences
International Journal of Biological Sciences 生物-生化与分子生物学
CiteScore
16.90
自引率
1.10%
发文量
413
审稿时长
1 months
期刊介绍: The International Journal of Biological Sciences is a peer-reviewed, open-access scientific journal published by Ivyspring International Publisher. It dedicates itself to publishing original articles, reviews, and short research communications across all domains of biological sciences.
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