دورية أكاديمية

Adiponectin suppresses tumor growth of nasopharyngeal carcinoma through activating AMPK signaling pathway

التفاصيل البيبلوغرافية
العنوان: Adiponectin suppresses tumor growth of nasopharyngeal carcinoma through activating AMPK signaling pathway
المؤلفون: Zhang, Zongmeng, Du, Jinlin, Shi, Hui, Wang, Shuai, Yan, Yunjing, Xu, Qihua, Zhou, Sujin, Zhao, Zhenggang, Mu, Yunping, Qian, Chaonan, Zhao, Allan Zijian, Cao, Sumei, Li, Fanghong
المساهمون: Key Research and Development Program of Guangdong Province, National Key Research and Development Program of China, National Natural Science Foundation of China, Guangdong Innovative Research Team Program, Startup R&D Funding of Guangdong University of Technology, Department of Education of Guangdong Province
المصدر: Journal of Translational Medicine ; volume 20, issue 1 ; ISSN 1479-5876
بيانات النشر: Springer Science and Business Media LLC
سنة النشر: 2022
مصطلحات موضوعية: General Biochemistry, Genetics and Molecular Biology, General Medicine
الوصف: Background Adiponectin is an adipocyte-secreted cytokine that enhances insulin sensitivity and attenuates inflammation. Although circulating adiponectin level is often inversely associated with several malignancies, its role in the development of nasopharyngeal carcinoma (NPC) remains unclear. Here, we investigated the clinical association between circulating adiponectin level and NPC, and examined the impact of adiponectin, as well as the underlying mechanisms, on NPC growth both in vitro and in vivo. Methods The association between circulating adiponectin level and the risk of developing NPC was assessed in two different cohorts, including a hospital-based case–control study with 152 cases and 132 controls, and a nested case–control study with 71 cases and 142 controls within a community-based NPC screening cohort. Tumor xenograft model, cell proliferation and cycle assays were applied to confirm the effects of adiponectin on NPC growth in cultured cells and in xenograft models. We also investigated the underlying signaling mechanisms with various specific pharmacological inhibitors and biochemistry analysis. Results High adiponectin levels were associated with a monotonic decreased trend of NPC risk among males in both the hospital-based case–control study and a nested case–control study. In vitro, recombinant human full-length adiponectin significantly inhibited NPC cell growth and arrested cell cycle, which were dependent on AMPK signaling pathway. The growth of xenograft of NPC tumor was sharply accelerated in the nude mice carrying genetic adiponectin deficiency. An adiponectin receptor agonist, AdipoRon, displayed strong anti-tumor activity in human xenograft models. Conclusions These findings demonstrated for the first time that circulating adiponectin is not only inversely associated with NPC, but also controls the development of NPC via AMPK signaling pathway. Stimulation of adiponectin function may become a novel therapeutic modality for NPC.
نوع الوثيقة: article in journal/newspaper
اللغة: English
DOI: 10.1186/s12967-022-03283-0
DOI: 10.1186/s12967-022-03283-0.pdf
DOI: 10.1186/s12967-022-03283-0/fulltext.html
الإتاحة: https://doi.org/10.1186/s12967-022-03283-0Test
حقوق: https://creativecommons.org/licenses/by/4.0Test ; https://creativecommons.org/licenses/by/4.0Test
رقم الانضمام: edsbas.D3054FAA
قاعدة البيانات: BASE