ArticleClinical & experimental metastasis2016
MCAM, as a novel receptor for S100A8/A9, mediates progression of malignant melanoma through prominent activation of NF-κB and ROS formation upon ligand binding.
Article in Clinical & experimental metastasis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 74 citations in OpenAlex.
- Remodeling the tumor dormancy ecosystem to prevent recurrence and metastasis.Signal transduction and targeted therapy · 2026Review
- Article
- S100A8/A9-MCAM signaling promotes gastric cancer cell progression via ERK-c-Jun activation.In vitro cellular & developmental biology. Animal · 2025Article
- Circulating Calprotectin Distinguishes Metastatic Melanoma and Predicts Liver Metastasis.International journal of molecular sciences · 2025Article
- Tumor Microenvironment in Melanoma Brain Metastasis: A New Potential Target?International journal of molecular sciences · 2025Review
- Lung-specific metastasis: the coevolution of tumor cells and lung microenvironment.Molecular cancer · 2025Review
- CD146 regulates the stemness and chemoresistance of hepatocellular carcinoma via JAG2-NOTCH signaling.Cell death & disease · 2025Article
- MCAM Expression Facilitates Melanoma-Endothelial Interactions and Promotes Metastatic Disease Progression.Experimental dermatology · 2025Article
- The RAGE Pathway in Skin Pathology Development: A Comprehensive Review of Its Role and Therapeutic Potential.International journal of molecular sciences · 2024Review
- Enhanced design of pCMViR-TSC plasmid vector for sustainably high cargo gene expression in mammalian cells.In vitro cellular & developmental biology. Animal · 2024Article
- Mcam stabilizes a luminal progenitor-like breast cancer cell state via Ck2 control and Src/Akt/Stat3 attenuation.NPJ breast cancer · 2024Article
- Contribution of Keratinocytes in Skin Cancer Initiation and Progression.International journal of molecular sciences · 2024Review
- ALCAM on human oligodendrocytes mediates CD4 T cell adhesion.Brain : a journal of neurology · 2024Article
- CD146 promotes resistance of NSCLC brain metastases to pemetrexed via the NF-κB signaling pathway.Frontiers in pharmacology · 2024Article
- CD146-targeted nuclear medicine imaging in cancer: state of the art.View (Beijing, China) · 2023Article
- Interaction of S100A6 Protein with the Four-Helical Cytokines.Biomolecules · 2023Article
- LOXL1 and LOXL4 are novel target genes of the ZnFrontiers in oncology · 2023Article
- The functions and regulatory pathways of S100A8/A9 and its receptors in cancers.Frontiers in pharmacology · 2023Review
- Lysyl oxidase-like 4 exerts an atypical role in breast cancer progression that is dependent on the enzymatic activity that targets the cell-surface annexin A2.Frontiers in oncology · 2023Article
- Galectin-3 Is a Natural Binding Ligand of MCAM (CD146, MUC18) in Melanoma Cells and Their Interaction Promotes Melanoma Progression.Biomolecules · 2022Article
Corrections and comments
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Authors and funding
17 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The dynamic interaction between tumor cells and their microenvironment induces a proinflammatory milieu that drives cancer development and progression. The S100A8/A9 complex has been implicated in chronic inflammation, tumor development, and progression. The cancer microenvironment contributes to the up-regulation of this protein complex in many invasive tumors, which is associated with the formation of pre-metastatic niches and poor prognosis. Changing adhesive preference of cancer cells is at the core of the metastatic process that governs the reciprocal interactions of cancer cells with the extracellular matrices and neighboring stromal cells. Cell adhesion molecules (CAMs) have been confirmed to have high-level expression in various highly invasive tumors. The expression and function of CAMs are profoundly influenced by the extracellular milieu. S100A8/A9 mediates its effects by binding to cell surface receptors, such as heparan sulfate, TLR4 and RAGE on immune and tumor cells. RAGE has recently been identified as an adhesion molecule and has considerably high identity and similarity to ALCAM and MCAM, which are frequently over-expressed on metastatic malignant melanoma cells. In this study, we demonstrated that ALCAM and MCAM also function as S100A8/A9 receptors as does RAGE and induce malignant melanoma progression by NF-κB activation and ROS formation. Notably, MCAM not only activated NF-κB more prominently than ALCAM and RAGE did but also mediated intracellular signaling for the formation of lung metastasis. MCAM is known to be involved in malignant melanoma development and progression through several mechanisms. Therefore, MCAM is a potential effective target in malignant melanoma treatment.
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