ArticleMolecular oncology2022
Role of L1CAM in retinoblastoma tumorigenesis: identification of novel therapeutic targets.
Article in Molecular oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Selection Signatures and Genetic Divergence in Hotan Black and F2 Yeonsan Ogye Chickens.Animals : an open access journal from MDPI · 2026Article
- B7-H3 and GD2 overexpression as immunotherapeutic targets in retinoblastoma.Scientific reports · 2026Article
- Clinical Significance of Soluble L1CAM Serum Levels in Patients with High-Risk Endometrial Cancer.Biomedicines · 2025Article
- α5-nAChR/ADAM10 signaling mediates nicotine-related cutaneous melanoma progression via STAT3 activation.Archives of dermatological research · 2024Article
- Role of Protein Tyrosine Phosphatase Receptor Type E (PTPRE) in Chemoresistant Retinoblastoma.International journal of molecular sciences · 2024Article
- Exosomal miR-214-3p from senescent osteoblasts accelerates endothelial cell senescence.Journal of orthopaedic surgery and research · 2023Article
- Tumor Suppressor Role of INPP4B in Chemoresistant Retinoblastoma.Journal of oncology · 2023Article
- ADAM10 and ADAM17-Novel Players in Retinoblastoma Carcinogenesis.International journal of molecular sciences · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The study presented focuses on the role of the neuronal cell adhesion molecule L1 cell adhesion molecule (L1CAM) in retinoblastoma (RB), the most common malignant intraocular childhood tumor. L1CAM is differentially expressed in a variety of human cancers and has been suggested as a promising therapeutic target. We likewise observed differential expression patterns for L1CAM in RB cell lines and patient samples. The two proteases involved in ectodomain shedding of L1CAM (L1CAM sheddases: ADAM10 and ADAM17) were likewise differentially expressed in the RB cell lines investigated, and an involvement in L1CAM processing in RB cells could be verified. We also identified ezrin, galectin-3, and fibroblast growth factor basic as L1CAM signaling target genes in RB cells. Lentiviral L1CAM knockdown induced apoptosis and reduced cell viability, proliferation, growth, and colony formation capacity of RB cells, whereas L1CAM-overexpressing RB cells displayed the opposite effects. Chicken chorioallantoic membrane assays revealed that L1CAM depletion decreases the tumorigenic and migration potential of RB cells in vivo. Moreover, L1CAM depletion decreased viability and tumor growth of etoposide-resistant RB cell lines upon etoposide treatment in vitro and in vivo. Thus, L1CAM and its processing sheddases are potential novel targets for future therapeutic RB approaches.
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