Ebp1 p48通过PI3K/Akt信号通路促进非小细胞肺癌的致癌特性

IF 2.8 4区 医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY
OncoTargets and therapy Pub Date : 2025-09-22 eCollection Date: 2025-01-01 DOI:10.2147/OTT.S537306
Lina Ma, Shuyuan Wang, Jia Zhang, Mengyuan Xin, Dongyuan Xu, Lan Liu, Xiangdan Li
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引用次数: 0

摘要

目的:肺癌,尤其是非小细胞肺癌(NSCLC),在全球范围内具有很高的致死率。p48是erbb3结合蛋白1 (Ebp1)的长亚型,其潜在的致癌作用已在其他癌症中得到证实,但其对非小细胞肺癌的影响仍未得到证实。患者和方法:利用多个数据库比较Ebp1在正常肺和非小细胞肺癌中的表达。采用免疫组织化学染色检测Ebp1在两种组织中的表达。TCGA数据库评估Ebp1在NSCLC中的表达及其对总生存期的影响。在A549和PC9细胞中敲低Ebp1的表达,通过CCK-8、平板克隆集落、软琼脂集落生成实验和细胞周期实验检测Ebp1对细胞生长的影响。Scratch、transwell和体内实验也证实了Ebp1对肺癌细胞迁移、侵袭的影响。Western blot检测EMT及信号通路相关蛋白。结果:本研究显示,NSCLC中Ebp1 p48的表达水平明显升高。我们使用非小细胞肺癌组织微阵列技术发现Ebp1 p48表达与病理分级、淋巴结转移、临床分期和总生存期(OS)之间存在相关性。在非小细胞肺癌细胞中,敲低Ebp1 p48可显著抑制肿瘤细胞的生长、迁移、侵袭、上皮-间质转化(epithelial-mesenchymal transition, EMT)过程和细胞增殖。此外,Ebp1 p48的敲除降低了PI3K和Akt的磷酸化水平。结论:根据这些发现,Ebp1 p48在NSCLC中刺激PI3K/Akt信号通路,进而促进侵袭、迁移和增殖。因此,在非小细胞肺癌中,Ebp1 p48可能是一个前瞻性的治疗靶点,也是一个预测性的生物标志物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Ebp1 p48 Promotes Oncogenic Properties in Non-Small Cell Lung Cancer Through PI3K/Akt Signaling Pathways.

Purpose: Lung cancer, particularly non-small cell lung cancer (NSCLC), is highly deadly globally. The potential carcinogenic role of p48, a long isoform of ErbB3-binding protein 1 (Ebp1), is well established in other cancers, but its impact on NSCLC remains unconfirmed.

Patients and methods: Several databases were utilized to compare Ebp1 expression in normal lung and NSCLC. Immunohistochemical staining was employed to identify Ebp1 expression in both types of tissue. The TCGA database assessed Ebp1 expression in NSCLC and its impact on overall survival. Ebp1 expression was knocked down in A549 and PC9 cells, and the impact of Ebp1 on the cell growth was tested by CCK-8, plate clone colony, soft agar colony generation assay, and cell cycle assays. Scratch, transwell, and in vivo were also used to confirm the effects of Ebp1 on Lung cancer cells migration, invasion. Western blot detection of EMT and signal pathway-related proteins.

Results: This study revealed that NSCLC had significantly higher levels of Ebp1 p48 expression. We discovered a correlation between Ebp1 p48 expression and pathological grade, lymph node metastasis, clinical stage, and overall survival (OS) using NSCLC tissue microarrays. In vitro and in vivo tumor cell growth, migration, invasion, the epithelial-mesenchymal transition (EMT) process, and cell proliferation are all markedly suppressed when Ebp1 p48 is knocked down in NSCLC cells. Moreover, PI3K and Akt phosphorylation levels were decreased by Ebp1 p48 knockdown.

Conclusion: According to these findings, Ebp1 p48 stimulated the PI3K/Akt signaling pathway in NSCLC, which in turn facilitated invasion, migration, and proliferation. As a result, in NSCLC, Ebp1 p48 may be a prospective therapeutic target as well as a predictive biomarker.

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来源期刊
OncoTargets and therapy
OncoTargets and therapy BIOTECHNOLOGY & APPLIED MICROBIOLOGY-ONCOLOGY
CiteScore
9.70
自引率
0.00%
发文量
221
审稿时长
1 months
期刊介绍: OncoTargets and Therapy is an international, peer-reviewed journal focusing on molecular aspects of cancer research, that is, the molecular diagnosis of and targeted molecular or precision therapy for all types of cancer. The journal is characterized by the rapid reporting of high-quality original research, basic science, reviews and evaluations, expert opinion and commentary that shed novel insight on a cancer or cancer subtype. Specific topics covered by the journal include: -Novel therapeutic targets and innovative agents -Novel therapeutic regimens for improved benefit and/or decreased side effects -Early stage clinical trials Further considerations when submitting to OncoTargets and Therapy: -Studies containing in vivo animal model data will be considered favorably. -Tissue microarray analyses will not be considered except in cases where they are supported by comprehensive biological studies involving multiple cell lines. -Biomarker association studies will be considered only when validated by comprehensive in vitro data and analysis of human tissue samples. -Studies utilizing publicly available data (e.g. GWAS/TCGA/GEO etc.) should add to the body of knowledge about a specific disease or relevant phenotype and must be validated using the authors’ own data through replication in an independent sample set and functional follow-up. -Bioinformatics studies must be validated using the authors’ own data through replication in an independent sample set and functional follow-up. -Single nucleotide polymorphism (SNP) studies will not be considered.
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