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CPEB2通过MEK/ERK信号通路影响TNBC恶性进展的研究

CPEB2 affects the malignant progression of TNBC through MEK/ERK signaling pathway

  • 摘要: 目的:探究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CPEB2在乳腺癌中的表达水平,利用免疫组化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=136.25,P<0.001)。高表达CPEB2患者OS显著高于低表达者。过表达CPEB2后抑制三阴性乳腺癌增殖、迁移、侵袭能力,并激活MEK/ERK信号通路。结论:CPEB2在三阴性乳腺癌中表达下调,其过表达可激活MEK/ERK信号通路抑制TNBC细胞的增殖、迁移及侵袭能力。

     

    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 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 = 136.25, P < 0.001). Patients with high expression of CPEB2 had a significantly longer overall survival (OS) than those with low expression. Overexpression of CPEB2 inhibited the proliferation, migration and invasion abilities of TNBC cells and activated the MEK/ERK signaling pathway. Conclusion: The expression of CPEB2 is downregulated in TNBC, and its overexpression can activate the MEK/ERK signaling pathway to inhibit the proliferation, migration and invasion abilities of TNBC cells.

     

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