ARPC1A is regulated by STAT3 to inhibit ferroptosis and promote prostate cancer progression.

IF 4.3 3区生物学 Human Cell Pub Date : 2022-09-01 Epub Date: 2022-07-23 DOI:10.1007/s13577-022-00754-w

Junpeng Ji, Huibing Li, Wenjun Wang, Bo Yuan, Tianyu Shen

{"title":"ARPC1A is regulated by STAT3 to inhibit ferroptosis and promote prostate cancer progression.","authors":"Junpeng Ji, Huibing Li, Wenjun Wang, Bo Yuan, Tianyu Shen","doi":"10.1007/s13577-022-00754-w","DOIUrl":null,"url":null,"abstract":"<p><p>The aim of this study was to investigate the biological function and molecular mechanism of ARPC1A (actin related protein 2/3 complex subunit 1A) in prostate cancer progression. RT-qPCR and IHC results showed that the level of ARPC1A in prostate cancer tissues was significantly higher than that in adjacent tissues. The results of TCGA (the cancer genome atlas) database analysis showed that high expression of ARPC1A indicates poor prognosis in prostate cancer patients. In vitro functional experiments confirmed that downregulation of ARPC1A expression resulted in decreased cell viability and invasive ability of prostate cancer cells, as ARPC1A knockdown promoted ferroptosis. The transcriptional regulation mechanism of STAT3 (signal transduction and activators of transcription 3) on ARPC1A was elucidated by Co-IP, ChIP and luciferase reporter assays. In vivo experiments also supported the in vitro results. We propose that reduced ARPC1A expression inhibits prostate cancer cell viability and invasion in a ferroptotic manner. The ARPC1A level may serve as an independent predictor of prognosis in prostate cancer patients.</p>","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 5","pages":"1591-1601"},"PeriodicalIF":4.3000,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"4","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Human Cell","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s13577-022-00754-w","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2022/7/23 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}

引用次数: 4

Abstract

The aim of this study was to investigate the biological function and molecular mechanism of ARPC1A (actin related protein 2/3 complex subunit 1A) in prostate cancer progression. RT-qPCR and IHC results showed that the level of ARPC1A in prostate cancer tissues was significantly higher than that in adjacent tissues. The results of TCGA (the cancer genome atlas) database analysis showed that high expression of ARPC1A indicates poor prognosis in prostate cancer patients. In vitro functional experiments confirmed that downregulation of ARPC1A expression resulted in decreased cell viability and invasive ability of prostate cancer cells, as ARPC1A knockdown promoted ferroptosis. The transcriptional regulation mechanism of STAT3 (signal transduction and activators of transcription 3) on ARPC1A was elucidated by Co-IP, ChIP and luciferase reporter assays. In vivo experiments also supported the in vitro results. We propose that reduced ARPC1A expression inhibits prostate cancer cell viability and invasion in a ferroptotic manner. The ARPC1A level may serve as an independent predictor of prognosis in prostate cancer patients.

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

ARPC1A受STAT3调控，抑制铁下垂，促进前列腺癌进展。

本研究旨在探讨ARPC1A(肌动蛋白相关蛋白2/3复合物亚基1A)在前列腺癌进展中的生物学功能和分子机制。RT-qPCR和免疫组化结果显示，ARPC1A在前列腺癌组织中的表达水平明显高于癌旁组织。TCGA (cancer genome atlas)数据库分析结果显示，ARPC1A高表达预示前列腺癌患者预后较差。体外功能实验证实，下调ARPC1A表达可导致前列腺癌细胞的细胞活力和侵袭能力下降，ARPC1A敲低可促进铁下垂。通过Co-IP、ChIP和荧光素酶报告基因检测，阐明了STAT3(信号转导和转录激活因子3)对ARPC1A的转录调控机制。体内实验也支持了体外实验结果。我们提出，ARPC1A表达的减少以铁致性的方式抑制前列腺癌细胞的活力和侵袭。ARPC1A水平可作为前列腺癌患者预后的独立预测因子。

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分钟内获得全文去求助

来源期刊

Human Cell 生物-细胞生物学

CiteScore

6.60

自引率

2.30%

发文量

176

期刊介绍： Human Cell is the official English-language journal of the Japan Human Cell Society. The journal serves as a forum for international research on all aspects of the human cell, encompassing not only cell biology but also pathology, cytology, and oncology, including clinical oncology. Embryonic stem cells derived from animals, regenerative medicine using animal cells, and experimental animal models with implications for human diseases are covered as well. Submissions in any of the following categories will be considered: Research Articles, Cell Lines, Rapid Communications, Reviews, and Letters to the Editor. A brief clinical case report focusing on cellular responses to pathological insults in human studies may also be submitted as a Letter to the Editor in a concise and short format. Not only basic scientists but also gynecologists, oncologists, and other clinical scientists are welcome to submit work expressing new ideas or research using human cells.