ArticleMolecular cancer research : MCR2018
Malignant Phenotypes in Metastatic Melanoma are Governed by SR-BI and its Association with Glycosylation and STAT5 Activation.
Article in Molecular cancer research : MCR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Dysregulation of SCARB1 Alternative Splicing Disturbs Amino Acid Metabolism in Anembryonic Pregnancy.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- STAT1/3/5 Functions Driving Lipid and Energy Metabolism in Cancer and Immunity.International journal of molecular sciences · 2026Review
- Capillary Endothelial Cells as Therapeutic Target in Pressure Overload-Induced Heart Failure.JACC. Basic to translational science · 2025Article
- Expression of the cholesterol transporter SR-B1 in melanoma cells facilitates inflammatory signaling leading to reduced cholesterol synthesis.Neoplasia (New York, N.Y.) · 2025Article
- IL-15 secreted by keratinocytes induces melanogenesis through STAT3/5 signaling pathway in melan-a melanocytes.Archives of dermatological research · 2025Article
- SOCS2 inhibits hepatoblastoma metastasis via downregulation of the JAK2/STAT5 signal pathway.Scientific reports · 2023Article
- Dysregulated cholesterol regulatory genes in hepatocellular carcinoma.European journal of medical research · 2023Review
- STAT5 confers lactogenic properties in breast tumorigenesis and restricts metastatic potential.Oncogene · 2022Article
- Emerging Roles of Post-Translational Modifications in Skin Diseases: Current Knowledge, Challenges and Future Perspectives.Journal of inflammation research · 2022Review
- High Density Lipoproteins: Is There a Comeback as a Therapeutic Target?Handbook of experimental pharmacology · 2022Article
- HDL and Scavenger Receptor Class B Type I (SRBI).Advances in experimental medicine and biology · 2022Review
- Review
- Aberrant Cholesterol Metabolism in Ovarian Cancer: Identification of Novel Therapeutic Targets.Frontiers in oncology · 2021Review
- Lipid metabolic Reprogramming: Role in Melanoma Progression and Therapeutic Perspectives.Cancers · 2020Review
- Cross-Talk between Inflammatory Mediators and the Epithelial Mesenchymal Transition Process in the Development of Thyroid Carcinoma.International journal of molecular sciences · 2019Review
- N-Glycosylation in progression of skin cancer.Medical oncology (Northwood, London, England) · 2019Review
- Loss of SR-BI Down-Regulates MITF and Suppresses Extracellular Vesicle Release in Human Melanoma.International journal of molecular sciences · 2019Article
- SR-BI Interactome Analysis Reveals a Proviral Role for UGGT1 in Hepatitis C Virus Entry.Frontiers in microbiology · 2019Article
- Scavenger receptor BI promotes cytoplasmic accumulation of lipoproteins in clear-cell renal cell carcinoma.Journal of lipid research · 2018Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Metastatic melanoma is hallmarked by elevated glycolytic flux and alterations in cholesterol homeostasis. The contribution of cholesterol transporting receptors for the maintenance of a migratory and invasive phenotype is not well defined. Here, the scavenger receptor class B type I (SCARB1/SR-BI), a high-density lipoprotein (HDL) receptor, was identified as an estimator of melanoma progression in patients. We further aimed to identify the SR-BI-controlled gene expression signature and its related cellular phenotypes. On the basis of whole transcriptome analysis, it was found that SR-BI knockdown, but not functional inhibition of its cholesterol-transporting capacity, perturbed the metastasis-associated epithelial-to-mesenchymal transition (EMT) phenotype. Furthermore, SR-BI knockdown was accompanied by decreased migration and invasion of melanoma cells and reduced xenograft tumor growth. STAT5 is an important mediator of the EMT process and loss of SR-BI resulted in decreased glycosylation, reduced DNA binding, and target gene expression of STAT5. When human metastatic melanoma clinical specimens were analyzed for the abundance of SR-BI and STAT5 protein, a positive correlation was found. Finally, a novel SR-BI-regulated gene profile was determined, which discriminates metastatic from nonmetastatic melanoma specimens indicating that SR-BI drives gene expression contributing to growth at metastatic sites. Overall, these results demonstrate that SR-BI is a highly expressed receptor in human metastatic melanoma and is crucial for the maintenance of the metastatic phenotype.
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Registered trials
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