CPEB2通过MEK/ERK信号通路影响TNBC恶性进展

木尼热·阿布拉; 李宇翔; 吴涛

doi:10.3971/j.issn.1000-8578.2026.25.0808

CPEB2通过MEK/ERK信号通路影响TNBC恶性进展

CPEB2 Affects Malignant Progression of TNBC Through MEK/ERK Signaling Pathway

摘要

摘要:
目的探讨CPEB2在三阴性乳腺癌中的表达及对肿瘤恶性进展的影响。
方法数据库分析乳腺癌中CPEB2的表达水平，利用免疫组织化学实验验证其在临床病理标本中的差异表达；构建CPEB2过表达三阴性乳腺癌稳转细胞系，使用CCK8、Transwell实验检测细胞表型变化，Western blot探索MEK/ERK信号通路关键分子表达。
结果三阴性乳腺癌癌组织中CPEB2表达显著低于癌旁组织（χ²=16.57，P<0.001）。CPEB2高表达者的OS显著高于低表达者。过表达CPEB2可抑制三阴性乳腺癌增殖、迁移、侵袭能力，并抑制MEK/ERK信号通路激活。
结论 CPEB2在三阴性乳腺癌中表达下调；上调CPEB2可抑制TNBC细胞的增殖、迁移与侵袭，并随MEK/ERK通路活化水平下降（p-MEK、p-ERK降低），提示CPEB2可能通过调控MEK/ERK通路参与TNBC恶性进展。

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. CPEB2 overexpressing stable TNBC cell lines were constructed, and CCK8 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, and its overexpression can affect the MEK/ERK signaling pathway, thereby inhibiting the proliferation, migration, and invasion abilities of TNBC cells.

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