期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 23, 期 21, 页码 -出版社
MDPI
DOI: 10.3390/ijms232112729
关键词
adiponectin; nasopharyngeal carcinoma; metastasis; STAT3; NF-kappa B
资金
- Key Research and Development Program of Guangdong Province for Innovative drug creation [2019B020201015]
- National Key R&D Program of China [2018YFA0800603]
- National Natural Science Foundation of China [81630021, 82100064, 81872700, 82073625]
- Guangdong Innovative Research Team Program [2016ZT06Y432]
- Startup R&D Funding of Guangdong University of Technology [50010102]
- Key Research and Development Program of Guangdong Province [2019B020227003]
- Key Project of Department of Education of Guangdong Province [2020ZDZX1048]
Adiponectin has multiple effects including regulation of metabolism, inhibition of cancer growth, and suppression of nasopharyngeal carcinoma (NPC) metastasis. Activation of the adiponectin receptor may be a promising therapeutic strategy for NPC metastasis.
Adiponectin is an adipocytokine with anti-inflammatory and anticancer properties. Our previous study has shown that blood adiponectin levels were inversely correlated to the risk of nasopharyngeal carcinoma (NPC), and that adiponectin could directly suppress the proliferation of NPC cells. However, the effect of adiponectin on NPC metastasis remains unknown. Here, we revealed in clinical studies that serum adiponectin level was inversely correlated with tumor stage, recurrence, and metastasis in NPC patients, and that low serum adiponectin level also correlates with poor metastasis-free survival. Coculture with recombinant adiponectin suppressed the migration and invasion of NPC cells as well as epithelial-mesenchymal transition (EMT). In addition, recombinant adiponectin dampened the activation of NF-kappa B and STAT3 signaling pathways induced by adipocyte-derived proinflammatory factors such as leptin, IL-6, and TNF-alpha. Pharmacological activation of adiponectin receptor through its specific agonist, AdipoRon, largely stalled the metastasis of NPC cells. Taken together, these findings demonstrated that adiponectin could not only regulate metabolism and inhibit cancer growth, but also suppress the metastasis of NPC. Pharmacological activation of adiponectin receptor may be a promising therapeutic strategy to stall NPC metastasis and extend patients' survival.
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