Actin-related protein 2/3 complex subunit 1B promotes ovarian cancer progression by regulating the AKT/PI3K/mTOR signaling pathway.

IF 4.7 2区 医学 Q1 MEDICINE, GENERAL & INTERNAL
Journal of Translational Internal Medicine Pub Date : 2024-10-01 eCollection Date: 2024-09-01 DOI:10.2478/jtim-2024-0025
Miao Ke, Huimin Zhu, Yu Lin, Ying Zhang, Tao Tang, Yuhao Xie, Zhe-Sheng Chen, Xiaoyu Wang, Yuan Shen
{"title":"Actin-related protein 2/3 complex subunit 1B promotes ovarian cancer progression by regulating the AKT/PI3K/mTOR signaling pathway.","authors":"Miao Ke, Huimin Zhu, Yu Lin, Ying Zhang, Tao Tang, Yuhao Xie, Zhe-Sheng Chen, Xiaoyu Wang, Yuan Shen","doi":"10.2478/jtim-2024-0025","DOIUrl":null,"url":null,"abstract":"<p><strong>Background and objectives: </strong>Actin-related protein 2/3 complex subunit 1B (ARPC1B) is an essential subunit of the actin-related protein 2/3 (Arp2/3) complex. While there have been numerous research reports on Arp2/3 in relation to tumors, there needs to be more research on ARPC1B and its role in tumors, particularly at the pan-cancer level.</p><p><strong>Methods: </strong>Utilizing data from the cancer genome atlas (TCGA) and genotype-tissue expression (GTEx) databases, we analyzed ARPC1B expression differences in normal, tumor, and adjacent tissues, investigating its correlation with prognosis and clinical stages in various cancers. We conducted gene enrichment analysis and explored ARPC1B's connection to the tumor immune microenvironment and its impact on anti-tumor drug resistance. In addition, <i>in vivo</i> and <i>in vitro</i> experiments have also been carried out to find the mechanism of ARPC1B on ovarian cancer (OV) proliferation and invasion.</p><p><strong>Results: </strong>ARPC1B was highly expressed in 33 tumor types, suggesting its role as a tumor-promoting factor. Its expression correlated with poor prognosis and served as a clinical staging marker in over 10 tumor types. ARPC1B is implicated in various biological processes and signaling pathways, uniquely associated with tumor immunity, indicating immunosuppressive conditions in high-expression cases. High ARPC1B expression was linked to resistance to six anti-tumor drugs. Further experiments showed that ARPC1B can affect the proliferation, apoptosis, migration, and invasion of OV cells through the AKT/PI3K/mTOR pathway.</p><p><strong>Conclusion: </strong>ARPC1B is a biomarker for immune suppression, prognosis, clinical staging, and drug resistance, providing new insights for cancer therapeutics.</p>","PeriodicalId":51339,"journal":{"name":"Journal of Translational Internal Medicine","volume":"12 4","pages":"406-423"},"PeriodicalIF":4.7000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11444474/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Translational Internal Medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.2478/jtim-2024-0025","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/9/1 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
引用次数: 0

Abstract

Background and objectives: Actin-related protein 2/3 complex subunit 1B (ARPC1B) is an essential subunit of the actin-related protein 2/3 (Arp2/3) complex. While there have been numerous research reports on Arp2/3 in relation to tumors, there needs to be more research on ARPC1B and its role in tumors, particularly at the pan-cancer level.

Methods: Utilizing data from the cancer genome atlas (TCGA) and genotype-tissue expression (GTEx) databases, we analyzed ARPC1B expression differences in normal, tumor, and adjacent tissues, investigating its correlation with prognosis and clinical stages in various cancers. We conducted gene enrichment analysis and explored ARPC1B's connection to the tumor immune microenvironment and its impact on anti-tumor drug resistance. In addition, in vivo and in vitro experiments have also been carried out to find the mechanism of ARPC1B on ovarian cancer (OV) proliferation and invasion.

Results: ARPC1B was highly expressed in 33 tumor types, suggesting its role as a tumor-promoting factor. Its expression correlated with poor prognosis and served as a clinical staging marker in over 10 tumor types. ARPC1B is implicated in various biological processes and signaling pathways, uniquely associated with tumor immunity, indicating immunosuppressive conditions in high-expression cases. High ARPC1B expression was linked to resistance to six anti-tumor drugs. Further experiments showed that ARPC1B can affect the proliferation, apoptosis, migration, and invasion of OV cells through the AKT/PI3K/mTOR pathway.

Conclusion: ARPC1B is a biomarker for immune suppression, prognosis, clinical staging, and drug resistance, providing new insights for cancer therapeutics.

肌动蛋白相关蛋白 2/3 复合物亚基 1B 通过调节 AKT/PI3K/mTOR 信号通路促进卵巢癌的进展。
背景和目的:肌动蛋白相关蛋白2/3复合体亚基1B(ARPC1B)是肌动蛋白相关蛋白2/3(Arp2/3)复合体的一个重要亚基。虽然已有大量关于 Arp2/3 与肿瘤关系的研究报告,但还需要更多关于 ARPC1B 及其在肿瘤中作用的研究,特别是在泛癌症层面:利用癌症基因组图谱(TCGA)和基因型-组织表达(GTEx)数据库的数据,我们分析了ARPC1B在正常组织、肿瘤组织和邻近组织中的表达差异,研究了它与各种癌症的预后和临床分期的相关性。我们进行了基因富集分析,探讨了 ARPC1B 与肿瘤免疫微环境的联系及其对抗肿瘤药物耐药性的影响。此外,我们还进行了体内和体外实验,以寻找 ARPC1B 对卵巢癌(OV)增殖和侵袭的影响机制:结果:ARPC1B 在 33 种肿瘤类型中高表达,表明它是一种肿瘤促进因子。ARPC1B的表达与预后不良相关,可作为10多种肿瘤类型的临床分期标志物。ARPC1B 与多种生物过程和信号通路有关,与肿瘤免疫独特相关,表明在高表达病例中存在免疫抑制情况。ARPC1B 的高表达与六种抗肿瘤药物的耐药性有关。进一步的实验表明,ARPC1B可通过AKT/PI3K/mTOR通路影响OV细胞的增殖、凋亡、迁移和侵袭:结论:ARPC1B是免疫抑制、预后、临床分期和耐药性的生物标志物,为癌症治疗提供了新的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Journal of Translational Internal Medicine
Journal of Translational Internal Medicine MEDICINE, GENERAL & INTERNAL-
CiteScore
5.50
自引率
8.20%
发文量
41
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信