Journal
ONCOTARGET
Volume 8, Issue 25, Pages 41364-41378Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.17326
Keywords
oleate; PTX3; metastasis
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Funding
- Ministry of Science and Technology of Taiwan [NSC 102-2628-B-006-011-MY3, 105-2320-B-006-022-MY3]
- National Cheng Kung University [the Headquarters of University Advancement]
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The association between metabolic diseases and the risk of developing cancer is emerging. However, the impact of long pentraxin- 3 (PTX3) on dyslipidemia- associated tumor metastasis remains unknown. In this study, we found that oleate induced PTX3 expression and secretion through the activation of Akt/NF-kappa B pathway in head and neck squamous cell carcinomas (HNSCCs). The activation of NF-kappa B was essential for the oleate-induced stabilization of PTX3 mRNA. In addition, both the depletion of PTX3 and the inhibition of NF-kappa B significantly inhibited oleate-induced tumor cell migration and invasion. The enhancement of binding between tumor and endothelial cells was observed in oleate-treated cells but not in the depletion and neutralization of PTX3 with siPTX3 and anti-PTX3 antibodies, respectively. The levels of oleateinduced epithelial-mesenchymal transition (EMT) markers, such as vimentin and MMP-3, were significantly reduced in PTX3-depleted cells. Knocking down vimentin also repressed oleate-induced HNSCC invasion. Furthermore, the depletion of PTX3 blocked the oleate-primed metastatic seeding of tumor cells in the lungs. These results demonstrate that oleate enhances HNSCC metastasis through the PTX3/vimentin signaling axes. The inhibition of PTX3 could be a potential strategy for the treatment of dyslipidemia-mediated HNSCC metastasis.
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