ArticleCellular and molecular life sciences : CMLS2013
Suppressor of cytokine signaling 1 blocks mitosis in human melanoma cells.
Article in Cellular and molecular life sciences : CMLS, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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.
The trial behind it
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
13 citing papers in PubMed, 20 citations in OpenAlex.
- Targeting ubiquitination in disease and therapy.Signal transduction and targeted therapy · 2025Review
- Integrating cuproptosis- and ferroptosis-related gene signatures to predict prognosis, immunotherapy response, and drug sensitivity in patients with skin cutaneous melanoma.Frontiers in immunology · 2025Article
- SOCS1 and SOCS3 as key checkpoint molecules in the immune responses associated to skin inflammation and malignant transformation.Frontiers in immunology · 2024Review
- SOCS1 expression in cancer cells: potential roles in promoting antitumor immunity.Frontiers in immunology · 2024Article
- Bona Fide Tumor Suppressor Genes Hypermethylated in Melanoma: A Narrative Review.International journal of molecular sciences · 2021Review
- Genetic variants of SDCCAG8 and MAGI2 in mitosis-related pathway genes are independent predictors of cutaneous melanoma-specific survival.Cancer science · 2021Article
- Cytokine-Mediated Dysregulation of Signaling Pathways in the Pathogenesis of Multiple Myeloma.International journal of molecular sciences · 2020Review
- SOCS3 inhibits the pathological effects of IL-22 in non-melanoma skin tumor-derived keratinocytes.Oncotarget · 2017Article
- The role of cullin 5-containing ubiquitin ligases.Cell division · 2016Review
- Epigenetic markers in melanoma.Melanoma management · 2015Review
- Gene therapy with SOCS1 for gastric cancer induces G2/M arrest and has an antitumour effect on peritoneal carcinomatosis.British journal of cancer · 2015Article
- Epigenetic regulation in human melanoma: past and future.Epigenetics · 2015Review
- SOCS, inflammation, and cancer.JAK-STAT · 2013Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypermethylation of SOCS genes is associated with many human cancers, suggesting a role as tumor suppressors. As adaptor molecules for ubiquitin ligases, SOCS proteins modulate turnover of numerous target proteins. Few SOCS targets identified so far have a direct role in cell cycle progression; the mechanism by which SOCS regulate the cell cycle thus remains largely unknown. Here we show that SOCS1 overexpression inhibits in vitro and in vivo expansion of human melanoma cells, and that SOCS1 associates specifically with Cdh1, triggering its degradation by the proteasome. Cells therefore show a G1/S transition defect, as well as a secondary blockade in mitosis and accumulation of cells in metaphase. SOCS1 expression correlated with a reduction in cyclin D/E levels and an increase in the tumor suppressor p19, as well as the CDK inhibitor p53, explaining the G1/S transition defect. As a result of Cdh1 degradation, SOCS1-expressing cells accumulated cyclin B1 and securin, as well as apparently inactive Cdc20, in mitosis. Levels of the late mitotic Cdh1 substrate Aurora A did not change. These observations comprise a hitherto unreported mechanism of SOCS1 tumor suppression, suggesting this molecule as a candidate for the design of new therapeutic strategies for human melanoma.
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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.