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CPEB2通过MEK/ERK信号通路影响三阴性乳腺癌恶性进展

木尼热·阿布拉 李宇翔 吴涛

肿瘤防治研究2026,Vol.53Issue(5):366-373,8.
肿瘤防治研究2026,Vol.53Issue(5):366-373,8.DOI:10.3971/j.issn.1000-8578.2026.25.0808

CPEB2通过MEK/ERK信号通路影响三阴性乳腺癌恶性进展

CPEB2 Affects Malignant Progression of Triple-Negative Breast Cancer Through MEK/ERK Signaling Pathway

木尼热·阿布拉 1李宇翔 1吴涛1

作者信息

  • 1. 830011 乌鲁木齐,新疆医科大学附属肿瘤医院乳腺外科(一病区)
  • 折叠

摘要

Abstract

Objective To investigate the expression of CPEB2 in triple-negative breast cancer(TNBC)and its impact on the malignant progression of tumors.Methods The expression level of CPEB2 in breast cancer was analyzed through a database,and the differential expression in clinical pathological specimens was verified by immunohistochemical experiments.Stable CPEB2 overexpressing TNBC cell lines were constru-cted,and CCK-8 and Transwell assays were used to detect the changes in cell phenotypes.Western blot was used to explore the expression of key molecules in the MEK/ERK signaling pathway.Results The expr-ession of CPEB2 in TNBC tissues was significantly lower than that in adjacent tissues(χ2=16.57,P<0.001).Patients with high expression of CPEB2 had a significantly longer overall survival than those with low expr-ession.Overexpression of CPEB2 inhibited the proliferation,migration,and invasion abilities of TNBC cells and the activation of the MEK/ERK signaling pathway.Conclusion The expression of CPEB2 is downre-gulated in TNBC.Upregulation of CPEB2 inhibits the proliferation,migration,and invasion of TNBC cells,accompanied by decreased activation of the MEK/ERK pathway(reduced p-MEK and p-ERK levels),sugg-esting that CPEB2 may participate in the malignant progression of TNBC by regulating the MEK/ERK pathway.

关键词

三阴性乳腺癌/CPEB2/恶性进展/MEK/ERK信号通路

Key words

TNBC/CPEB2/Malignant progression/MEK/ERK signal transduction pathway

分类

医药卫生

引用本文复制引用

木尼热·阿布拉,李宇翔,吴涛..CPEB2通过MEK/ERK信号通路影响三阴性乳腺癌恶性进展[J].肿瘤防治研究,2026,53(5):366-373,8.

基金项目

Open Research Project of the Key Laboratory of Oncology in Xinjiang(No.XJKLO-2023U006) 新疆肿瘤学重点实验室开放课题(XJKLO-2023U006) (No.XJKLO-2023U006)

肿瘤防治研究

1000-8578

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