ArticleHereditas2025
Exploring MAP3K genes in gastric cancer: biomarkers, tumor microenvironment dynamics, and chemotherapy resistance.
Article in Hereditas, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- MAP3K1: A Multifunctional Kinase at the Crossroads of Cancer Progression and Tumor Suppression.Cells · 2026Review
- Bioinformatic analysis and experimental validation of the function of mitogen-activated protein kinase in esophageal cancer.Discover oncology · 2026Article
- Beyond COL1A1::PDGFB: Rare fusions and their clinical implications in dermatofibrosarcoma protuberans.World journal of clinical cases · 2025Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGastric cancer (GC) presents a significant global health burden, necessitating a deeper understanding of its molecular underpinnings for improved diagnostics and therapeutics.
methodsIn this study, we investigated the expression profiles and clinical implications of MAP3K genes in GC using in silico and in vitro experiments.
resultsUtilizing RT-qPCR analysis, we observed significant up-regulation of MAP3K1, MAP3K4, MAP3K5, MAP3K6, MAP3K7, MAP3K8, MAP3K9, and MAP3K10 in GC cell lines, while MAP3K2, MAP3K3, MAP3K11, MAP3K12, MAP3K13, MAP3K14, and MAP3K15 exhibited down-regulation. Prognostic evaluation revealed that elevated expression of MAP3K1, MAP3K4, MAP3K7, MAP3K8, MAP3K9, and MAP3K10 was associated with shorter overall survival (OS), emphasizing their clinical significance. Furthermore, the diagnostic potential was demonstrated through robust Receiver operating characteristics (ROC) curve analysis, indicating the strong discriminatory power of these genes in distinguishing GC patients. Proteomic analysis further confirmed the higher expression of MAP3K1, MAP3K4, MAP3K7, MAP3K8, MAP3K9, and MAP3K10 genes in GC. Methylation profiling further supported the idea that promoter hypomethylation of MAP3K1, MAP3K4, MAP3K7, MAP3K8, MAP3K9, and MAP3K10 genes was associated with their up-regulation. Single-cell functional analysis elucidated the involvement of MAP3K genes in shaping the tumor microenvironment. miRNA-mRNA network analysis revealed intricate regulatory mechanisms, with hsa-mir-200b-3p emerging as a key regulator. Finally, the MAP3K1 knockdown has shown significant impacts on the cellular behavior of the BGC823 cells.
conclusionThis comprehensive assessment provides valuable insights into the role of MAP3K genes in GC, offering avenues for further research and therapeutic exploration.
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