ARRB2 promotes cervical cancer progression via stabilizing CDC25A mRNA through m6A-IGF2BP1-dependent manner.

IF 6.8 1区医学 Q1 ONCOLOGY NPJ Precision Oncology Pub Date : 2025-03-21 DOI:10.1038/s41698-025-00862-4

Lijie Li, Jie Zeng, Mengying Liu, Hui Cheng, Yuyin He, Sili He, Chen Wang

{"title":"ARRB2 promotes cervical cancer progression via stabilizing CDC25A mRNA through m6A-IGF2BP1-dependent manner.","authors":"Lijie Li, Jie Zeng, Mengying Liu, Hui Cheng, Yuyin He, Sili He, Chen Wang","doi":"10.1038/s41698-025-00862-4","DOIUrl":null,"url":null,"abstract":"<p><p>Cervical cancer causes many deaths among women worldwide. Exploring the mechanisms underlying proliferation and metastasis contributes to developing novel intervention strategies. Here, we found that ARRB2 was highly expressed, and its increased expression was associated with poor prognosis of patients with cervical cancer. Knockdown of ARRB2 repressed the proliferation, migration, invasion and EMT of cervical cancer cells. Furthermore, CDC25A was upregulated, and ARRB2 stabilized CDC25A mRNA through IGF2BP1. CDC25A silencing inhibited proliferation, migration, and invasion, but it was reversed by ARRB2 overexpression. Silencing of CDC25A suppressed EMT signaling via promoting FOXO3 phosphorylation and cytoplasmic localization and inhibiting Snail1 transcription. Knockdown of ARRB2 suppressed tumor growth and metastasis through CDC25A downregulation. In conclusion, ARRB2 promotes FOXO3 nuclear translocation and Snail1 transcription by stabilizing CDC25A mRNA in an m6A-dependent manner, thus facilitating proliferation and metastasis in cervical cancer.</p>","PeriodicalId":19433,"journal":{"name":"NPJ Precision Oncology","volume":"9 1","pages":"80"},"PeriodicalIF":6.8000,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11928456/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"NPJ Precision Oncology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1038/s41698-025-00862-4","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ONCOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Cervical cancer causes many deaths among women worldwide. Exploring the mechanisms underlying proliferation and metastasis contributes to developing novel intervention strategies. Here, we found that ARRB2 was highly expressed, and its increased expression was associated with poor prognosis of patients with cervical cancer. Knockdown of ARRB2 repressed the proliferation, migration, invasion and EMT of cervical cancer cells. Furthermore, CDC25A was upregulated, and ARRB2 stabilized CDC25A mRNA through IGF2BP1. CDC25A silencing inhibited proliferation, migration, and invasion, but it was reversed by ARRB2 overexpression. Silencing of CDC25A suppressed EMT signaling via promoting FOXO3 phosphorylation and cytoplasmic localization and inhibiting Snail1 transcription. Knockdown of ARRB2 suppressed tumor growth and metastasis through CDC25A downregulation. In conclusion, ARRB2 promotes FOXO3 nuclear translocation and Snail1 transcription by stabilizing CDC25A mRNA in an m6A-dependent manner, thus facilitating proliferation and metastasis in cervical cancer.

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

ARRB2 通过 m6A-IGF2BP1 依赖性方式稳定 CDC25A mRNA，从而促进宫颈癌的进展。

宫颈癌导致全球许多妇女死亡。探索增殖和转移的内在机制有助于开发新的干预策略。在这里，我们发现 ARRB2 高表达，其表达增加与宫颈癌患者的不良预后有关。敲除 ARRB2 可抑制宫颈癌细胞的增殖、迁移、侵袭和 EMT。此外，CDC25A上调，ARRB2通过IGF2BP1稳定CDC25A mRNA。沉默 CDC25A 可抑制细胞的增殖、迁移和侵袭，但 ARRB2 的过表达可逆转这种情况。沉默 CDC25A 可通过促进 FOXO3 磷酸化和胞质定位以及抑制 Snail1 转录来抑制 EMT 信号转导。敲除RRB2可通过下调CDC25A抑制肿瘤的生长和转移。总之，ARRB2通过稳定CDC25A mRNA以m6A依赖的方式促进FOXO3核转位和Snail1转录，从而促进宫颈癌的增殖和转移。

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

NPJ Precision Oncology ONCOLOGY-

CiteScore

9.90

自引率

1.30%

发文量

审稿时长

18 weeks

期刊介绍： Online-only and open access, npj Precision Oncology is an international, peer-reviewed journal dedicated to showcasing cutting-edge scientific research in all facets of precision oncology, spanning from fundamental science to translational applications and clinical medicine.