ArticleOncogene2001
Increased susceptibility to tumorigenesis of ski-deficient heterozygous mice.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 85 citations in OpenAlex.
- Article
- The Anti-fibrosis drug Pirfenidone modifies the immunosuppressive tumor microenvironment and prevents the progression of renal cell carcinoma by inhibiting tumor autocrine TGF-β.Cancer biology & therapy · 2022Article
- Article
- SKI activates the Hippo pathway via LIMD1 to inhibit cardiac fibroblast activation.Basic research in cardiology · 2021Article
- Review
- Novel regulation of Ski protein stability and endosomal sorting by actin cytoskeleton dynamics in hepatocytes.The Journal of biological chemistry · 2015Article
- Ski regulates Hippo and TAZ signaling to suppress breast cancer progression.Science signaling · 2015Article
- c-Ski activates cancer-associated fibroblasts to regulate breast cancer cell invasion.Molecular oncology · 2013Article
- Ski protein levels increase during in vitro progression of HPV16-immortalized human keratinocytes and in cervical cancer.Virology · 2013Article
- Expression profiles of SnoN in normal and cancerous human tissues support its tumor suppressor role in human cancer.PloS one · 2013Article
- Ski inhibits TGF-β/phospho-Smad3 signaling and accelerates hypertrophic differentiation in chondrocytes.Journal of cellular biochemistry · 2012Article
- Overexpression of SKI oncoprotein leads to p53 degradation through regulation of MDM2 protein sumoylation.The Journal of biological chemistry · 2012Article
- Alterations in the Smad pathway in human cancers.Frontiers in bioscience (Landmark edition) · 2012Review
- Chromosomal instability in mouse embryonic fibroblasts null for the transcriptional co-repressor Ski.Journal of cellular physiology · 2012Article
- Identification of Ski as a target for Aurora A kinase.Biochemical and biophysical research communications · 2011Article
- Suppression of p53 activity through the cooperative action of Ski and histone deacetylase SIRT1.The Journal of biological chemistry · 2011Article
- Efficient TGF-β/SMAD signaling in human melanoma cells associated with high c-SKI/SnoN expression.Molecular cancer · 2011Article
- A two-gene signature, SKI and SLAMF1, predicts time-to-treatment in previously untreated patients with chronic lymphocytic leukemia.PloS one · 2011Article
- SKI promotes Smad3 linker phosphorylations associated with the tumor-promoting trait of TGFbeta.Cell cycle (Georgetown, Tex.) · 2010Article
- The phosphatidylinositol 3-kinase/Akt pathway regulates transforming growth factor-{beta} signaling by destabilizing ski and inducing Smad7.The Journal of biological chemistry · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
The c-ski proto-oncogene product (c-Ski) acts as a co-repressor and binds to other co-repressors N-CoR/SMRT and mSin3A which form a complex with histone deacetylase (HDAC). c-Ski mediates the transcriptional repression by a number of repressors, including nuclear hormone receptors and Mad. c-Ski also directly binds to, and recruits the HDAC complex to Smads, leading to inhibition of tumor growth factor-beta (TGF-beta) signaling. This is consistent with the function of ski as an oncogene. Here we show that loss of one copy of c-ski increases susceptibility to tumorigenesis in mice. When challenged with a chemical carcinogen, c-ski heterozygous mice showed an increased level of tumor formation relative to wild-type mice. In addition, c-ski-deficient mouse embryonic fibroblasts (MEFs) had increased proliferative capacity, whereas overexpression of c-Ski suppressed the proliferation. Furthermore, the introduction of activated Ki-ras into c-ski-deficient MEFs resulted in neoplastic transformation. These findings demonstrate that c-ski acts as a tumor suppressor in some types of cells. The level of cdc25A mRNA, which is down regulated by two tumor suppressor gene products, Rb and Mad, was upregulated in c-ski-deficient MEFs, whereas it decreased by overexpressing c-Ski in MEFs. This is consistent with the fact that c-Ski acts as a co-repressor of Mad and Rb. These results support the view that the decreased activities of Mad and Rb in ski-deficient cells at least partly contribute to enhanced proliferation and susceptibility to tumorigenesis. Human c-ski gene was mapped to a region close to the p73 tumor suppressor gene at the 1p36.3 locus, which is already known to contain multiple uncharacterized tumor suppressor genes.
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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.