ArticleAdipocyte2024
Leptin secreted by adipocytes promotes EMT transition and endometrial cancer progression via the JAK2/STAT3 signalling pathway.
Article in Adipocyte, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- The Gut-Adipose-Tumor Axis in Obesity-Related Cancer.Nutrients · 2026Review
- Obesity and Cancer: From Systemic Metabolic Reprogramming to Immunotherapy Paradox.Metabolites · 2026Review
- Reproductive integration of leptin and kisspeptin in small ruminants: Mechanisms, biomarker potential, and prospects for precision breeding.Veterinary world · 2025Review
- Present progress in biomarker discovery of endometrial cancer by multi-omics approaches.Clinical proteomics · 2025Review
- Complement activation at the interface between adipocytes and cancer cells drives tumor progression.JCI insight · 2025Article
- Unraveling the role of STAT3 in Cancer Cachexia: pathogenic mechanisms and therapeutic opportunities.Frontiers in endocrinology · 2025Review
- Targeting the leptin receptor promotes MDA-MB-231 cells' metabolic reprogramming and malignancy: the role of extracellular vesicles derived from obese adipose tissue.Frontiers in oncology · 2025Article
- Effect of adipocytes on the function and activity of T cells in tumor microenvironment.Frontiers in immunology · 2025Review
- Novel perspectives on the link between obesity and cancer risk: from mechanisms to clinical implications.Frontiers of medicine · 2024Review
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEndometrial cancer is a malignant tumour with a high incidence and mortality rate, and obesity is one of the most significant risk factors for the disease. However, it remains unclear whether leptin affects cell activity, proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). MATERIALS AND
methodsSamples of endometrial cancer tissue were obtained from clinical patients and nude mice Enzyme-linked immunosorbent assays (ELISAs) were performed to assess leptin levels. Western blotting, immunohistochemical (IHC) and immunofluorescence (IF) analyses were conducted to detect EMT, JAK2/STAT3 signalling pathway proteins, and cell proliferation biomarkers. Cell Counting Kit-8 (CCK-8) assays, 5-ethynyl-2'-deoxyuridine (EdU) staining, and Transwell assays were used to evaluate cell activity, proliferation, migration, and invasion, respectively.
resultsELISA, western blot and immunohistochemistry (IHC) analyses showed that leptin was highly expressed, and the JAK2/STAT3 signalling pathway was activated in endometrial cancer patients. Cell-based experiments showed that adipocytes secreted leptin, which increased the levels of leptin, and also promoted cell migration and invasion, EMT transition, and cell activity and proliferation. Leptin accelerated cell progression and promoted EMT via the JAK2/STAT3 signalling pathway in a dose-dependent manner. The tumour-promoting effect of leptin on endometrial cancer cells was further verified by
conclusionLeptin secreted by adipocytes promotes EMT transition and endometrial cancer progression via the JAK2/STAT3 signalling pathway in a dose-dependent manner.
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