PARP inhibitor olaparib induced differential protein expression in cervical cancer cells

奥拉帕尼 PARP抑制剂 聚ADP核糖聚合酶 蛋白质组 PARP1 癌症研究 生物 赫拉 合成致死 宫颈癌 癌细胞 DNA损伤 癌症 DNA损伤修复 化学 DNA修复 蛋白质组学 核糖核酸 分子生物学 小RNA 德罗沙 污渍 细胞 庆大霉素保护试验 细胞凋亡 程序性细胞死亡 信使核糖核酸 卵巢癌 细胞生物学 聚合酶
作者
Jyotika Rajawat,Poorwa Awasthi,Monisha Banerjee
出处
期刊:Journal of Proteomics [Elsevier BV]
卷期号:275: 104823-104823 被引量:2
标识
DOI:10.1016/j.jprot.2023.104823
摘要

PARP inhibitors are a potential class of chemotherapeutic drugs but PARP inhibitor response has not been explored systematically. We lack a specific understanding of the subset of the proteome preferentially modified in various cancers by PARP inhibitors. Implications of PARP inhibitor and PARP1 in cervical cancer treatment and resistance are not fully elucidated. We conducted a mass spectrometry-based proteomic analysis of cervical cancer Hela cells treated with olaparib. We aimed to identify the alteration in the protein signaling pathway induced by PARP inhibitors beyond the DNA damage response pathway. Our data demonstrate a significant reduction in PARP activity and enhanced cell death after olaparib treatment. We further observed articulated proteomic changes with a significant enrichment of proteins in diverse cellular processes. The differentially expressed proteins were predominantly associated with RNA metabolism, mRNA splicing, processing, and RNA binding. Our data also identified proteins that could probably contribute to survival mechanisms resulting in resistance to PARP inhibitors. Hence, we put forth the overview of proteomic changes induced by PARP inhibitor olaparib in cervical cancer cells. This study highlights the significant proteins modified during PARP inhibition and thus could be a probable target for combination therapies with PARP inhibitors in cervical cancer. This study provides the overview of proteomic changes induced by PARP inhibitor olaparib in cervical cancer Hela cells. We demonstrated that Olaparib inhibited PARP1 activity in Hela cells in a dose-dependent manner while no change was observed in the expression of PARP1. PARP inhibition potentially regulated the RNA metabolism, RNA binding proteins, metastasis-related genes, mitochondrial proteins, transcription factors and regulators, and ubiquitination proteins. We also identified increased expression of tumor-promoting and drug resistance proteins that could contribute to the resistance mechanism to PARPi therapy. This approach will be helpful to generate insights into precision oncology for personalized treatment and generate data repositories for future artificial intelligence-based research.
最长约 10秒,即可获得该文献文件

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
hhh完成签到 ,获得积分10
1秒前
落落完成签到 ,获得积分10
2秒前
ty完成签到 ,获得积分10
3秒前
lling完成签到 ,获得积分10
9秒前
肯德鸭完成签到,获得积分10
13秒前
Nancy0818完成签到 ,获得积分0
16秒前
guoxihan完成签到,获得积分10
16秒前
坦率绮山完成签到 ,获得积分10
23秒前
小天小天完成签到 ,获得积分10
23秒前
lzq671完成签到 ,获得积分10
23秒前
白昼完成签到 ,获得积分10
27秒前
27秒前
无花果应助科研通管家采纳,获得10
28秒前
可爱沛蓝完成签到 ,获得积分10
30秒前
37秒前
hyishu完成签到,获得积分10
39秒前
江南第八完成签到,获得积分10
39秒前
Pursue完成签到,获得积分10
40秒前
Willa发布了新的文献求助10
40秒前
百事可爱完成签到 ,获得积分10
41秒前
美满惜寒完成签到,获得积分10
43秒前
CGBIO完成签到,获得积分10
43秒前
44秒前
guoyufan完成签到,获得积分10
44秒前
王jyk完成签到,获得积分10
44秒前
Syan完成签到,获得积分10
44秒前
洋芋饭饭完成签到,获得积分10
44秒前
朝夕之晖完成签到,获得积分10
45秒前
tingting完成签到,获得积分10
45秒前
ys1008完成签到,获得积分10
45秒前
喜喜完成签到,获得积分10
45秒前
675完成签到,获得积分10
45秒前
runtang完成签到,获得积分10
46秒前
prrrratt完成签到,获得积分10
46秒前
qq完成签到,获得积分10
46秒前
cityhunter7777完成签到,获得积分10
46秒前
呵呵哒完成签到,获得积分10
46秒前
Temperature完成签到,获得积分10
47秒前
张浩林完成签到,获得积分10
47秒前
啪嗒大白球完成签到,获得积分10
47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
Introduction to Helicopter and Tiltrotor Flight Simulation, Second Edition 2500
Developing Genetic Editing Tools for Lysobacter 2000
卤化钙钛矿人工突触的研究 2000
Моделирование процессов самоорганизации в кристаллообразующих системах 1000
History of U.S. Space Surveillance and Satellite Cataloging 1000
Malcolm Fraser : a biography 700
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 物理 内科学 复合材料 催化作用 物理化学 光电子学 电极 细胞生物学 基因 无机化学
热门帖子
关注 科研通微信公众号,转发送积分 6512356
求助须知:如何正确求助?哪些是违规求助? 8305790
关于积分的说明 17742143
捐赠科研通 5613975
什么是DOI,文献DOI怎么找? 2923772
邀请新用户注册赠送积分活动 1901024
关于科研通互助平台的介绍 1762725