Journal
CANCERS
Volume 14, Issue 23, Pages -Publisher
MDPI
DOI: 10.3390/cancers14236003
Keywords
nasopharyngeal carcinoma; resistin; TLR4; metastasis; NF-kappa B
Categories
Funding
- Key Research and Development Program of Guangdong Province for Innovative drug creation
- National Key R&D Program of China [2019B020201015]
- National Natural Science Foundation of China [2018YFA0800603]
- Guangdong Innovative Research Team Program [81630021, 82100064, 81872700, 82073625]
- Startup R&D Funding of the Guangdong University of Technology [2016ZT06Y432]
- Key Research and Development Program of Guangdong Province [50010102]
- Key Project of the Department of Education of Guangdong Province [2019B020227003]
- [2020ZDZX1048]
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Chronic inflammation is associated with the development of nasopharyngeal carcinoma (NPC), where resistin, an inflammatory cytokine, plays a role in promoting tumor metastasis. High resistin levels in NPC patients are positively correlated with lymph node metastasis, and resistin induces epithelial-mesenchymal transition (EMT) to facilitate metastasis. The TLR4/p38 MAPK/NF-kappa B signaling pathways are involved in resistin-mediated promotion of NPC metastasis.
Simple SummaryChronic inflammation is associated with the development of nasopharyngeal carcinoma (NPC). Mounting evidence has indicated that resistin is an inflammatory cytokine that is associated with the risk of tumorigenesis. However, the correlation between serum resistin levels and the risk of NPC remains unclear. Here, we found that high serum resistin levels in NPC patients were positively correlated with lymph node metastasis and that resistin promoted the metastasis of NPC cells both in vitro and in vivo. Furthermore, we elucidated the underlying molecular mechanisms through which resistin promotes metastasis in NPC cells by inducing the epithelial-mesenchymal transition (EMT).NPC is a type of malignant tumor with a high risk of local invasion and early distant metastasis. Resistin is an inflammatory cytokine that is predominantly produced from the immunocytes in humans. Accumulating evidence has suggested a clinical association of circulating resistin with the risk of tumorigenesis and a relationship between blood resistin levels and the risk of cancer metastasis. In this study, we explored the blood levels and the role of resistin in NPC. High resistin levels in NPC patients were positively associated with lymph node metastasis, and resistin promoted the migration and invasion of NPC cells in vitro. These findings were also replicated in a mouse model of NPC tumor metastasis. We identified TLR4 as a functional receptor in mediating the pro-migratory effects of resistin in NPC cells. Furthermore, p38 MAPK and NF-kappa B were intracellular effectors that mediated resistin-induced EMT. Taken together, our results suggest that resistin promotes NPC metastasis by activating the TLR4/p38 MAPK/NF-kappa B signaling pathways.
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