Lina Ma, Shuyuan Wang, Jia Zhang, Mengyuan Xin, Dongyuan Xu, Lan Liu, Xiangdan Li
{"title":"Ebp1 p48 Promotes Oncogenic Properties in Non-Small Cell Lung Cancer Through PI3K/Akt Signaling Pathways.","authors":"Lina Ma, Shuyuan Wang, Jia Zhang, Mengyuan Xin, Dongyuan Xu, Lan Liu, Xiangdan Li","doi":"10.2147/OTT.S537306","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose: </strong>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.</p><p><strong>Patients and methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"1093-1105"},"PeriodicalIF":2.8000,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12474717/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"OncoTargets and therapy","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.2147/OTT.S537306","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"BIOTECHNOLOGY & APPLIED MICROBIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
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.
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.