ArticleScientific reports2018
Alternative splicing of ALCAM enables tunable regulation of cell-cell adhesion through differential proteolysis.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Defining the Functional Role and Potential as an Immunotherapeutic Target of ALCAM in Neuroblastoma.Molecular cancer therapeutics · 2026Article
- Epigenetic drivers of metalloproteinases and metastasis.Trends in cell biology · 2025Review
- Article
- Alternative splicing regulation and its therapeutic potential in bladder cancer.Frontiers in oncology · 2024Review
- The function of alternative splicing in the proteome: rewiring protein interactomes to put old functions into new contexts.Nature structural & molecular biology · 2023Review
- Protrusion growth driven by myosin-generated force.Developmental cell · 2023Article
- The Clinical and Theranostic Values of Activated Leukocyte Cell Adhesion Molecule (ALCAM)/CD166 in Human Solid Cancers.Cancers · 2021Review
- Comparative proteomics analysis indicates that palmatine contributes to transepithelial migration by regulating cellular adhesion.Pharmaceutical biology · 2020Article
- To cut or not to cut: New rules for proteolytic shedding of membrane proteins.The Journal of biological chemistry · 2020Article
- Negatively charged amino acids in the stalk region of membrane proteins reduce ectodomain shedding.The Journal of biological chemistry · 2020Article
- Modulation of cell adhesion and migration through regulation of the immunoglobulin superfamily member ALCAM/CD166.Clinical & experimental metastasis · 2019Review
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
While many adhesion receptors are known to influence tumor progression, the mechanisms by which they dynamically regulate cell-cell adhesion remain elusive. We previously identified Activated Leukocyte Cell Adhesion Molecule (ALCAM) as a clinically relevant driver of metastasis and hypothesized that a tunable mechanism of ectodomain shedding regulates its contribution to dissemination. To test this hypothesis, we examined an under-explored ALCAM splice variant (ALCAM-Iso2) and demonstrated that loss of the membrane-proximal region of ALCAM (exon 13) increased metastasis four-fold. Mechanistic studies identified a novel MMP14-dependent membrane distal cleavage site in ALCAM-Iso2, which mediated a ten-fold increase in shedding, thereby decreasing cellular cohesion. Importantly, the loss of cohesion is not limited to the cell capable of shedding because the released extracellular domain diminished cohesion of non-shedding cells through disruption of ALCAM-ALCAM interactions. ALCAM-Iso2-dominated expression in bladder cancer tissue, compared to normal bladder, further emphasizes that ALCAM alternative splicing may contribute to clinical disease progression. The requirement for both the loss of exon 13 and the gain of metalloprotease activity suggests that ALCAM shedding and concomitant regulation of tumor cell adhesion is a locally tunable process.
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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.