ArticleCancer research2014
ALCAM/CD166 is a TGF-β-responsive marker and functional regulator of prostate cancer metastasis to bone.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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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
52 citing papers in PubMed, 85 citations in OpenAlex.
- Low-PSMA hormone-sensitive prostate cancer: a distinct clinical and molecular state.Molecular medicine (Cambridge, Mass.) · 2026Article
- Article
- Integrating single-cell analysis and digital pathology for risk stratification in pancreatic cancer.Clinical & experimental metastasis · 2026Article
- Defining the Functional Role and Potential as an Immunotherapeutic Target of ALCAM in Neuroblastoma.Molecular cancer therapeutics · 2026Article
- Review
- GATA2 up-regulation restores androgen receptor chromatin association and advances darolutamide resistance in prostate cancer.Genes & diseases · 2025Article
- Epithelial-to-mesenchymal transition (EMT) and cancer metastasis: the status quo of methods and experimental models 2025.Molecular cancer · 2025Review
- SCGB3A1-Epi and KLK10-Epi Crosstalk With Fibroblasts Promotes Liver Metastasis of Breast Cancer and Pancreatic Ductal Adenocarcinoma.Cancer medicine · 2025Article
- Patient-Derived Colorectal Cancer Extracellular Matrices Modulate Cancer Cell Stemness Markers.International journal of molecular sciences · 2025Article
- TGF-β1-mediated intercellular signaling fuels cooperative cellular invasion.Cell reports · 2025Article
- Cross-Talk between the TGF-β and Cell Adhesion Signaling Pathways in Cancer.International journal of medical sciences · 2024Review
- sBioSITe enables sensitive identification of the cell surface proteome through direct enrichment of biotinylated peptides.Clinical proteomics · 2023Article
- Tissue-specific cancer stem/progenitor cells: Therapeutic implications.World journal of stem cells · 2023Review
- Exploration of diagnostic biomarkers, microenvironment characteristics, and ursolic acid's therapeutic effect for benign prostate hyperplasia.International journal of biological sciences · 2023Article
- Proteome profiling of enzalutamide-resistant cell lines and serum analysis identified ALCAM as marker of resistance in castration-resistant prostate cancer.International journal of cancer · 2022Article
- Gene variation impact on prostate cancer progression: Lymphocyte modulator, activation, and cell adhesion gene variant contribution.The Prostate · 2022Article
- Review
- Advancing Treatment of Bone Metastases through Novel Translational Approaches Targeting the Bone Microenvironment.Cancers · 2022Review
- Prostate Cancer Stem Cells: Clinical Aspects and Targeted Therapies.Frontiers in oncology · 2022Review
- ALCAM-EGFR interaction regulates myelomagenesis.Blood advances · 2021Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
The dissemination of prostate cancer to bone is a common, incurable aspect of advanced disease. Prevention and treatment of this terminal phase of prostate cancer requires improved molecular understanding of the process as well as markers indicative of molecular progression. Through biochemical analyses and loss-of-function in vivo studies, we demonstrate that the cell adhesion molecule, activated leukocyte cell adhesion molecule (ALCAM), is actively shed from metastatic prostate cancer cells by the sheddase ADAM17 in response to TGF-β. Not only is this posttranslational modification of ALCAM a marker of prostate cancer progression, the molecule is also required for effective metastasis to bone. Biochemical analysis of prostate cancer cell lines reveals that ALCAM expression and shedding is elevated in response to TGF-β signaling. Both in vitro and in vivo shedding is mediated by ADAM17. Longitudinal analysis of circulating ALCAM in tumor-bearing mice revealed that shedding of tumor, but not host-derived ALCAM is elevated during growth of the cancer. Gene-specific knockdown of ALCAM in bone-metastatic PC3 cells greatly diminished both skeletal dissemination and tumor growth in bone. The reduced growth of ALCAM knockdown cells corresponded to an increase in apoptosis (caspase-3) and decreased proliferation (Ki67). Together, these data demonstrate that the ALCAM is both a functional regulator as well as marker of prostate cancer 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.