ArticleJournal of cell science2010
Nuclear factor-kappaB signaling and ezrin are essential for L1-mediated metastasis of colon cancer cells.
Article in Journal of cell science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.
- L1 Cell Adhesion Molecule in Cancer, a Systematic Review on Domain-Specific Functions.International journal of molecular sciences · 2019Pooled it
- The value and application of a poorly differentiated cluster-based Ezrin marginal score system in the prognostic assessment of colorectal cancer.Discover oncology · 2025Article
- A Necessary Role for Cyclin D2 Induction During Colon Cancer Progression Mediated by L1.Cells · 2024Article
- Single-Cell RNA Sequencing (scRNA-seq) Identifies L1CAM as a Key Mediator between Epithelial Tuft Cell and Innate Lymphoid Cell in the Colon ofBiomedicines · 2023Article
- Review
- Mice Mutated in the Third Fibronectin Domain of L1 Show Enhanced Hippocampal Neuronal Cell Death, Astrogliosis and Alterations in Behavior.Biomolecules · 2023Article
- Cytoskeletal and Cytoskeleton-Associated Proteins: Key Regulators of Cancer Stem Cell Properties.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Downregulation of the Tumor Suppressor TFF1 Is Required during Induction of Colon Cancer Progression by L1.Cancers · 2022Article
- Targeting the Ezrin Adaptor Protein Sensitizes Metastatic Breast Cancer Cells to Chemotherapy and Reduces Neoadjuvant Therapy-induced Metastasis.Cancer research communications · 2022Article
- A Necessary Role for Increased Biglycan Expression during L1-Mediated Colon Cancer Progression.International journal of molecular sciences · 2021Article
- Article
- Neuroglian regulates Drosophila intestinal stem cell proliferation through enhanced signaling via the epidermal growth factor receptor.Stem cell reports · 2021Article
- The Collagen-Modifying Enzyme PLOD2 Is Induced and Required during L1-Mediated Colon Cancer Progression.International journal of molecular sciences · 2021Article
- Portrait of Cancer Stem Cells on Colorectal Cancer: Molecular Biomarkers, Signaling Pathways and miRNAome.International journal of molecular sciences · 2021Review
- Nodal-induced L1CAM/CXCR4 subpopulation sustains tumor growth and metastasis in colorectal cancer derived organoids.Theranostics · 2021Article
- Review
- L1CAM is involved in lymph node metastasis via ERK1/2 signaling in colorectal cancer.American journal of translational research · 2020Article
- Ezrin Mediates Invasion and Metastasis in Tumorigenesis: A Review.Frontiers in cell and developmental biology · 2020Review
- ISG15 induction is required during L1-mediated colon cancer progression and metastasis.Oncotarget · 2019Article
- Increased expression of cathepsin D is required for L1-mediated colon cancer progression.Oncotarget · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
Hyperactivation of beta-catenin-T-cell-factor (TCF)-regulated gene transcription is a hallmark of colorectal cancer (CRC). The cell-neural adhesion molecule L1CAM (hereafter referred to as L1) is a target of beta-catenin-TCF, exclusively expressed at the CRC invasive front in humans. L1 overexpression in CRC cells increases cell growth and motility, and promotes liver metastasis. Genes induced by L1 are also expressed in human CRC tissue but the mechanisms by which L1 confers metastasis are still unknown. We found that signaling by the nuclear factor kappaB (NF-kappaB) is essential, because inhibition of signaling by the inhibitor of kappaB super repressor (IkappaB-SR) blocked L1-mediated metastasis. Overexpression of the NF-kappaB p65 subunit was sufficient to increase CRC cell proliferation, motility and metastasis. Binding of the L1 cytodomain to ezrin - a cytoskeleton-crosslinking protein - is necessary for metastasis because when binding to L1 was interrupted or ezrin gene expression was suppressed with specific shRNA, metastasis did not occur. L1 and ezrin bound to and mediated the phosphorylation of IkappaB. We also observed a complex containing IkappaB, L1 and ezrin in the juxtamembrane region of CRC cells. Furthermore, we found that L1, ezrin and phosphorylated p65 are co-expressed at the invasive front in human CRC tissue, indicating that L1-mediated activation of NF-kappaB signaling involving ezrin is a major route of CRC progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.