CPEB2 Affects Malignant Progression of Triple-Negative Breast Cancer Through MEK/ERK Signaling Pathway
10.3971/j.issn.1000-8578.2026.25.0808
- VernacularTitle:CPEB2通过MEK/ERK信号通路影响三阴性乳腺癌恶性进展
- Author:
Yuxiang LI
1
;
Tao WU
1
Author Information
1. Department of Breast Surgery (Ward 1), Tumor Hospital Affiliated to Xinjiang Medical University, Urumqi 830011, China.
- Collective Name:Munire·abula
- Publication Type:CLINICALRESEARCH
- Keywords:
TNBC;
CPEB2;
Malignant progression;
MEK/ERK signal transduction pathway
- From:
Cancer Research on Prevention and Treatment
2026;53(5):366-373
- CountryChina
- Language:Chinese
-
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 constructed, 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 expression 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 expression. 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 downregulated 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), suggesting that CPEB2 may participate in the malignant progression of TNBC by regulating the MEK/ERK pathway.
