ArticleCancer genomics & proteomics
Analysis of Protein-Protein Interactions Identifies NECTIN2 as a Target of
Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- A synthetic benzoxazine dimer derivative targets c-Myc to inhibit colorectal cancer progression.Molecular oncology · 2026Article
- ST6GalNAc-I regulates tumor cell sialylation via NECTIN2/MUC5AC-mediated immunosuppression and angiogenesis in non-small cell lung cancer.The Journal of clinical investigation · 2025Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimMetastasis negatively affects the survival of lung cancer patients, however, relatively few compounds have potential in metastasis suppression. This study investigated the molecular targets of N,N-bis (5-ethyl-2-hydroxybenzyl) methylamine (EMD) for metastatic inhibition. MATERIALS AND
methodsProteins were analyzed by proteomic and bioinformatic analyses. Protein-protein interaction (PPI) networks were created with the Search Tool for the Retrieval of Interacting Genes. The Kyoto Encyclopedia of Genes and Genomes database and hub genes were used to determine dominant pathways. Immunofluorescence and western blot analyses validated the proteomic results and investigated signaling pathways in NCI-H23 lung cancer cells.
resultsA total of 1,751 proteins were common to the control, EMD and N,N-bis(5-methoxy-2-hydroxybenzyl) methylamine (MeMD) groups; 1,980 different proteins were categorized using metastatic capacity category and analyzed for unique proteins affected by EMD. Fifteen proteins were associated with cell adhesion and six with cell migration. Nectin cell adhesion molecule 2 (NECTIN2) was expressed in the control and MeMD-treated groups but not the EMD-treated group, suggesting NECTIN2 as an EMD target. PPI network showed association of NECTIN2 with proteins regulating cancer metastasis. Kyoto Encyclopedia of Genes and Genomes pathways revealed that NECTIN2 is an upstream target of cytoskeletal regulation via SRC signaling. Western blot and immunofluorescence analyses confirmed that EMD suppressed NECTIN2, and its downstream targets, including p-SRC (Y146 and Y527) and the epithelial-to-mesenchymal transition markers tight junction protein 1, vimentin, β-catenin, snail family transcriptional repressor 1 (SNAI1), and SNAI2, while increasing E-cadherin.
conclusionEMD suppressed NECTIN2-induced activation of EMT signaling. These data support the development of EMD to prevent metastasis of lung cancer.
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Registered trials
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