■子宫内膜癌是一种发病率和死亡率都很高的恶性肿瘤,肥胖是该疾病最重要的危险因素之一。然而,目前尚不清楚瘦素是否会影响细胞活性,扩散,迁移,入侵,和上皮-间质转化(EMT)。
■从临床患者和裸鼠获得子宫内膜癌组织的样品。进行酶联免疫吸附测定(ELISA)以评估瘦素水平。西方印迹,进行免疫组织化学(IHC)和免疫荧光(IF)分析以检测EMT,JAK2/STAT3信号通路蛋白,和细胞增殖生物标志物。细胞计数试剂盒-8(CCK-8)测定,5-乙炔基-2'-脱氧尿苷(EdU)染色,和Transwell分析用于评估细胞活性,扩散,迁移,和入侵,分别。
■ELISA,蛋白质印迹和免疫组织化学(IHC)分析显示,瘦素高表达,子宫内膜癌患者的JAK2/STAT3信号通路被激活。基于细胞的实验表明,脂肪细胞分泌瘦素,增加了瘦素的水平,并促进细胞迁移和侵袭,EMT过渡,细胞活性和增殖。瘦素通过JAK2/STAT3信号通路以剂量依赖性方式加速细胞进展并促进EMT。通过体内实验进一步验证了瘦素对子宫内膜癌细胞的促肿瘤作用,其中瘦素促进肿瘤生长并激活JAK2/STAT3信号通路。
■脂肪细胞分泌的瘦素通过JAK2/STAT3信号通路以剂量依赖性方式促进EMT转变和子宫内膜癌进展。子宫内膜癌患者具有高水平的瘦素通过JAK2/STAT3信号通路促进EMT转变瘦素通过JAK2/STAT3信号通路促进子宫内膜癌进展瘦素以剂量依赖性方式促进子宫内膜癌。
Endometrial 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).
Samples 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.
ELISA, 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 in vivo experiments, in which leptin promoted tumour growth and activated the JAK2/STAT3 signalling pathway.
Leptin secreted by adipocytes promotes EMT transition and endometrial cancer progression via the JAK2/STAT3 signalling pathway in a dose-dependent manner.Highlights Endometrial cancer patients have high levels of leptinLeptin promotes EMT transition via the JAK2/STAT3 signalling pathwayLeptin promotes endometrial cancer progression via the JAK2/STAT3 signalling pathwayLeptin promotes endometrial cancer in a dose-dependent manner.