NUSAP1 Binds ILF2 to Modulate R-Loop Accumulation and DNA Damage in Prostate Cancer

生物 DNA损伤 相互作用体 计算生物学 蛋白质组学 DNA 细胞生物学 遗传学 基因
作者
Chun-Lung Chiu,Caiyun G. Li,Erik Verschueren,Ru Wen,Dalin Zhang,Catherine A. Gordon,Hongjuan Zhao,Amato J. Giaccia,James D. Brooks
出处
期刊:International Journal of Molecular Sciences [MDPI AG]
卷期号:24 (7): 6258-6258 被引量:5
标识
DOI:10.3390/ijms24076258
摘要

Increased expression of NUSAP1 has been identified as a robust prognostic biomarker in prostate cancer and other malignancies. We have previously shown that NUSAP1 is positively regulated by E2F1 and promotes cancer invasion and metastasis. To further understand the biological function of NUSAP1, we used affinity purification and mass spectrometry proteomic analysis to identify NUSAP1 interactors. We identified 85 unique proteins in the NUSAP1 interactome, including ILF2, DHX9, and other RNA-binding proteins. Using proteomic approaches, we uncovered a function for NUSAP1 in maintaining R-loops and in DNA damage response through its interaction with ILF2. Co-immunoprecipitation and colocalization using confocal microscopy verified the interactions of NUSAP1 with ILF2 and DHX9, and RNA/DNA hybrids. We showed that the microtubule and charged helical domains of NUSAP1 were necessary for the protein-protein interactions. Depletion of ILF2 alone further increased camptothecin-induced R-loop accumulation and DNA damage, and NUSAP1 depletion abolished this effect. In human prostate adenocarcinoma, NUSAP1 and ILF2 mRNA expression levels are positively correlated, elevated, and associated with poor clinical outcomes. Our study identifies a novel role for NUSAP1 in regulating R-loop formation and accumulation in response to DNA damage through its interactions with ILF2 and hence provides a potential therapeutic target.

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
燕燕于飞发布了新的文献求助10
刚刚
刚刚
Hello应助Lina采纳,获得10
2秒前
2秒前
lxl完成签到,获得积分10
2秒前
4秒前
4秒前
4秒前
4秒前
正直纸飞机完成签到,获得积分10
6秒前
one完成签到,获得积分10
6秒前
7秒前
DagrZheng完成签到,获得积分10
7秒前
CodeCraft应助科研通管家采纳,获得10
7秒前
CodeCraft应助科研通管家采纳,获得10
7秒前
小蘑菇应助科研通管家采纳,获得10
7秒前
小蘑菇应助科研通管家采纳,获得10
7秒前
Hello应助科研通管家采纳,获得10
8秒前
Hello应助科研通管家采纳,获得10
8秒前
8秒前
8秒前
8秒前
8秒前
无极微光应助科研通管家采纳,获得20
8秒前
无极微光应助科研通管家采纳,获得20
8秒前
8秒前
小二郎应助科研通管家采纳,获得10
8秒前
小二郎应助科研通管家采纳,获得10
8秒前
李健应助科研通管家采纳,获得10
8秒前
李健应助科研通管家采纳,获得10
8秒前
爆米花应助科研通管家采纳,获得10
9秒前
9秒前
9秒前
9秒前
9秒前
9秒前
9秒前
9秒前
Owen应助科研通管家采纳,获得10
9秒前
chino发布了新的文献求助30
9秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Encyclopedia of Quaternary Science Reference Third edition 6000
Encyclopedia of Forensic and Legal Medicine Third Edition 5000
Agyptische Geschichte der 21.30. Dynastie 2000
Processing of reusable surgical textiles for use in health care facilities 500
Population genetics 2nd edition 500
工学基礎離散数学とその応用[第2版] 500
热门求助领域 (近24小时)
化学 材料科学 生物 医学 工程类 计算机科学 有机化学 物理 生物化学 纳米技术 复合材料 内科学 化学工程 人工智能 催化作用 遗传学 数学 基因 量子力学 物理化学
热门帖子
关注 科研通微信公众号,转发送积分 5807600
求助须知:如何正确求助?哪些是违规求助? 5864170
关于积分的说明 15521689
捐赠科研通 4932262
什么是DOI,文献DOI怎么找? 2655828
邀请新用户注册赠送积分活动 1602377
关于科研通互助平台的介绍 1557419