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Pinosylvin inhibits migration and invasion of nasopharyngeal carcinoma cancer cells via regulation of epithelial-mesenchymal transition and inhibition of MMP-2

Nasopharyngeal carcinoma (NPC) is a tumor located in the nasopharynx with highly invasive and metastatic properties. Metastasis is a primary cause of mortality in patients with NPC. The terpenoid polyphenol pinosylvin is a known functional compound of the Pinus species that exhibits anti-inflammator...

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Detalles Bibliográficos
Autores principales: Chuang, Yi-Ching, Hsieh, Ming-Chang, Lin, Chia-Chieh, Lo, Yu-Sheng, Ho, Hsin-Yu, Hsieh, Ming-Ju, Lin, Jen-Tsun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8165580/
https://www.ncbi.nlm.nih.gov/pubmed/34080661
http://dx.doi.org/10.3892/or.2021.8094
Descripción
Sumario:Nasopharyngeal carcinoma (NPC) is a tumor located in the nasopharynx with highly invasive and metastatic properties. Metastasis is a primary cause of mortality in patients with NPC. The terpenoid polyphenol pinosylvin is a known functional compound of the Pinus species that exhibits anti-inflammatory effects; however, the effect of pinosylvin on human NPC cell migration and invasion is unclear. The present study aimed to investigate the functional role of pinosylvin in NPC cells (NPC-039, NPC-BM and RPMI 2650). Gap closure and Transwell assay indicated that pinosylvin at increasing concentrations inhibited migration and invasion of NPC-039 and NPC-BM cells. In addition to inhibiting the enzyme activity of MMP-2, pinosylvin also decreased the protein expression levels of MMP-2 and MMP-9. Pinosylvin decreased the expression of vimentin and N-cadherin and significantly increased the expression of zonula occludens-1 and E-cadherin in NPC cells. Additionally, pinosylvin suppressed the invasion and migration ability of NPC-039 and NPC-BM cells by mediating the p38, ERK1/2 and JNK1/2 pathways. The present results revealed that pinosylvin inhibited migration and invasion in NPC cells.