ArticleInternational journal of molecular sciences2021
The Collagen-Modifying Enzyme PLOD2 Is Induced and Required during L1-Mediated Colon Cancer Progression.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- Salvianolic Acid B Inhibited LH2 Expression to Reduce Collagen Synthesis in Pulmonary Fibrosis.Journal of cellular and molecular medicine · 2026Article
- A Necessary Role for Cyclin D2 Induction During Colon Cancer Progression Mediated by L1.Cells · 2024Article
- Article
- Integrative single-cell and bulk transcriptomes analyses reveals heterogeneity of serine-glycine-one-carbon metabolism with distinct prognoses and therapeutic vulnerabilities in HNSCC.International journal of oral science · 2024Article
- Integrins as the pivotal regulators of cisplatin response in tumor cells.Cell communication and signaling : CCS · 2024Review
- An Increase in Mucin2 Expression Is Required for Colon Cancer Progression Mediated by L1.International journal of molecular sciences · 2023Article
- PLOD2 promotes colorectal cancer progression by stabilizing USP15 to activate the AKT/mTOR signaling pathway.Cancer science · 2023Article
- METTL3-ModulatedCancers · 2023Article
- Identification of lactylation related model to predict prognostic, tumor infiltrating immunocytes and response of immunotherapy in gastric cancer.Frontiers in immunology · 2023Article
- Apelin promotes osteosarcoma metastasis by upregulating PLOD2 expression via the Hippo signaling pathway and hsa_circ_0000004/miR-1303 axis.International journal of biological sciences · 2023Article
- Ivermectin Affects Neutrophil-Induced Inflammation through Inhibition of Hydroxylysine but Stimulation of Cathepsin G and Phenylalanine Secretion.Biomedicines · 2022Article
- Downregulation of the Tumor Suppressor TFF1 Is Required during Induction of Colon Cancer Progression by L1.Cancers · 2022Article
- Silencing PLOD2 attenuates cancer stem cell-like characteristics and cisplatin-resistant through Integrin β1 in laryngeal cancer.Translational oncology · 2022Article
- PLOD Family: A Novel Biomarker for Prognosis and Personalized Treatment in Soft Tissue Sarcoma.Genes · 2022Article
- Proteomics profiling of colorectal cancer progression identifies PLOD2 as a potential therapeutic target.Cancer communications (London, England) · 2022Article
- PLOD2 high expression associates with immune infiltration and facilitates cancer progression in osteosarcoma.Frontiers in oncology · 2022Article
- A Necessary Role for Increased Biglycan Expression during L1-Mediated Colon Cancer Progression.International journal of molecular sciences · 2021Article
- Clinical Prognostic Value of theFrontiers in molecular biosciences · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The overactivation of Wnt/β-catenin signaling is a hallmark of colorectal cancer (CRC) development. We identified the cell adhesion molecule L1CAM (L1) as a target of β-catenin-TCF transactivation in CRC cells. The overexpression of L1 in CRC cells confers enhanced proliferation, motility, tumorigenesis and liver metastasis, and L1 is exclusively localized in the invasive areas of human CRC tissue. A number of genes are induced after L1 transfection into CRC cells by a mechanism involving the cytoskeletal protein ezrin and the NF-κB pathway. When studying the changes in gene expression in CRC cells overexpressing L1 in which ezrin levels were suppressed by shRNA to ezrin, we discovered the collagen-modifying enzyme lysyl hydroxylase 2 (PLOD2) among these genes. We found that increased PLOD2 expression was required for the cellular processes conferred by L1, including enhanced proliferation, motility, tumorigenesis and liver metastasis, since the suppression of endogenous PLOD2 expression, or its enzymatic activity, blocked the enhanced tumorigenic properties conferred by L1. The mechanism involved in increased PLOD2 expression by L1 involves ezrin signaling and PLOD2 that affect the SMAD2/3 pathway. We found that PLOD2 is localized in the colonic crypts in the stem cell compartment of the normal mucosa and is found at increased levels in invasive areas of the tumor and, in some cases, throughout the tumor tissue. The therapeutic strategies to target PLOD2 expression might provide a useful approach for CRC treatment.
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