The DOI matches its Crossref record; 39 of the 40 references it cites were found in a registry or an index.
STAT3-mediated constitutive expression of SOCS-3 in cutaneous T-cell lymphoma
Abstract
A characteristic feature of neoplastic transformation is the loss of external control by cytokines and extracellular matrix of cellular differentiation, migration, and mitogenesis. Because suppressors of cytokine signaling (SOCS) proteins are negative regulators of cytokine-induced signaling, it has been hypothesized that an aberrant SOCS expression plays a role in neoplastic transformation. This study reports on a constitutive SOCS-3 expression in cutaneous T-cell lymphoma (CTCL) cell lines. SOCS-3 protein is constitutively expressed in tumor cell lines (but not in nonmalignant T cells) obtained from affected skin from a patient with mycosis fungoides (MF) and from peripheral blood from a patient with Sezary syndrome (SS). In contrast, constitutive SOCS-3 expression is not found in the leukemic Jurkat T-cell line, the MOLT-4 acute lymphoblastic leukemia cell line, and the monocytic leukemic cell line U937. Expression of SOCS-3 coincides with a constitutive activation of STAT3 in CTCL tumor cells, and stable transfection of CTCL tumor cells with a dominant negative STAT3 strongly inhibits SOCS-3 expression, whereas transfection with wild-type STAT3 does not. Moreover, the reduced SOCS-3 expression in cells transfected with the dominant negative STAT3 is associated with an increased sensitivity to interferon-alpha (IFN-alpha). In conclusion, evidence is provided for a constitutive SOCS-3 expression in cancer cells obtained from patients with CTCL. Moreover, the findings indica…
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“activated STAT3 induces SOCS3 expression, the protein product of which inhibits Janus kinases (JAKs) responsible for phosphorylating STAT3”
From Dynamic IL-6R/STAT3 signaling leads to heterogeneity of metabolic phenotype in pancreatic ductal adenocarcinoma cells (2024) · cites this paper as [39]
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Metadata
- Authors
- Brender, C., Nielsen, M., Kaltoft, K., Mikkelsen, G., Zhang, Q., Wasik, M., Billestrup, N., & Ødum, N.
- Affiliations
- University of Copenhagen (DK)
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2001-02-15
- Volume
- 97
- Issue
- 4
- Pages
- 1056-1062
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2020666846
- Cited by
- 129
- References
- 40
- Citations by year
- 2024: 1 · 2023: 4 · 2022: 1 · 2021: 3 · 2020: 2 · 2019: 6 · 2018: 4 · 2017: 3 · 2016: 4 · 2015: 4 · 2014: 6 · 2013: 4 · 2012: 11
- FWCI
- 11.56
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Blood (publishedVersion)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Funders
- National Cancer Institute (CA 89194, R01CA089194)
- Topics
- Health Sciences › Medicine › Dermatology › Cutaneous lymphoproliferative disorders research
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Keywords
- SOCS3, STAT3, cutaneous T-cell lymphoma, mycosis fungoides, Sézary syndrome, constitutive expression, dominant-negative STAT3, suppressor of cytokine signaling, oncogenic transformation, cytokine signaling
- MeSH terms
- Suppressor of Cytokine Signaling 3 Protein, Cell Transformation, Neoplastic, Dimethyl Sulfoxide, DNA-Binding Proteins, Enzyme Inhibitors, Genes, Dominant, Humans, Interferon-gamma, Mutation, Mycosis Fungoides, Neoplasm Proteins, Proteins, Quinazolines, Recombinant Fusion Proteins, Repressor Proteins, RNA, Messenger, RNA, Neoplasm, Sezary Syndrome, Skin Neoplasms, Transcription Factors, Transcription, Genetic, Transfection, Protein Biosynthesis, Tumor Cells, Cultured, Leukemia-Lymphoma, Adult T-Cell, Trans-Activators, Gene Expression Regulation, Neoplastic, Interferon-alpha, Jurkat Cells, Tyrphostins, STAT3 Transcription Factor, Suppressor of Cytokine Signaling Proteins
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