ArticleOncogene2014
Enhancement of leptin receptor signaling by SOCS3 deficiency induces development of gastric tumors in mice.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Prognostic Significance of SOCS3 in Patients With Solid Tumors: A Meta-Analysis.Frontiers in surgery · 2021Pooled it
- TFF3 initiates gastric intestinal metaplasia by activating JAK2 and STAT3 under high salt conditions.Scientific reports · 2025Article
- Diet, Gastric Microbiota, and Metabolites in Gastric Tumorigenesis.Research (Washington, D.C.) · 2025Review
- E3 ligase SOCS3 regulates NOD2 expression by ubiquitin proteasome system in lung cancer progression.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Article
- The Immune Response in Adipocytes and Their Susceptibility to Infection: A Possible Relationship with Infectobesity.International journal of molecular sciences · 2022Review
- Multi-omics reveals microbiome, host gene expression, and immune landscape in gastric carcinogenesis.iScience · 2022Article
- Knockdown of miR-92a suppresses the stemness of colorectal cancer cells via mediating SOCS3.Bioengineered · 2022Article
- Altered microbiota by a high-fat diet accelerates lethal myeloid hematopoiesis associated with systemic SOCS3 deficiency.iScience · 2021Article
- SOCS3 Expression by Thymic Stromal Cells Is Required for Normal T Cell Development.Frontiers in immunology · 2021Article
- The Adipokine Component in the Molecular Regulation of Cancer Cell Survival, Proliferation and Metastasis.Pathology oncology research : POR · 2021Review
- High fat diet, gut microbiome and gastrointestinal cancer.Theranostics · 2021Review
- New Actors Driving the Epithelial-Mesenchymal Transition in Cancer: The Role of Leptin.Biomolecules · 2020Review
- Dysregulated circulating SOCS3 and haptoglobin expression associated with stable coronary artery disease and acute coronary syndrome: An integrated study based on bioinformatics analysis and case-control validation.Anatolian journal of cardiology · 2020Article
- Dietary Restriction Suppresses Steatosis-Associated Hepatic Tumorigenesis in Hepatitis C Virus Core Gene Transgenic Mice.Liver cancer · 2020Article
- Article
- Identification of SOCS family members with prognostic values in human ovarian cancer.American journal of translational research · 2020Article
- Leptin signaling impairs macrophage defenses againstProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Gastric Leptin and Tumorigenesis: Beyond Obesity.International journal of molecular sciences · 2019Review
- Programmable Base Editing of the Sheep Genome Revealed No Genome-Wide Off-Target Mutations.Frontiers in genetics · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leptin acts on its receptor (ObR) in the hypothalamus to inhibit food intake and energy expenditure. Leptin and ObR are also expressed in the gastrointestinal tract; however, the physiological significance of leptin signaling in the gut remains uncertain. Suppressor of cytokine signaling 3 (SOCS3) is a key negative feedback regulator of ObR-mediated signaling in the hypothalamus. We now show that gastrointestinal epithelial cell-specific SOCS3 conditional knockout (T3b-SOCS3 cKO) mice developed gastric tumors by enhancing leptin production and the ObRb/signal transducer and activator of transcription 3 (STAT3) signaling pathway. All T3b-SOCS3 cKO mice developed tumors in the stomach but not in the bowels by 2 months of age, even though the SOCS3 deletion occurred in both the epithelium of stomach and bowels. The tumors developed in the absence of the inflammatory response and all cKO mice died within 6 months. These tumors displayed pathology and molecular alterations, such as an increase in MUC2 (Mucin 2, oligomeric mucus/gel-forming) and TFF3 (trefoil factor 3), resembling human intestinal-type gastric tumors. Administration of antileptin antibody to T3b-SOCS3 cKO mice reduced hyperplasia of gastric mucosa, which is the step of the initiation of gastric tumor. These data suggest that SOCS3 is an antigastric tumor gene that suppresses leptin overexpression and ObRb/STAT3 hyperactivation, supporting the hypothesis that the leptin/ObRb/STAT3 axis accelerates tumorigenesis and that it may represent a new therapeutic target for the treatment of gastric cancer.
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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.