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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.

ABSTRACT: 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.

SUBMITTER: Chuang YC

PROVIDER: S-EPMC8165580 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundTo examine whether MLKL participated in the invasion of radiosensitive nasopharyngeal carcinoma (NPC) cell (CNE-2) and radioresistant NPC cell (CR) through regulating epithelial-mesenchymal transition (EMT).MethodssiRNA and CRISPR/Cas9 technique were used to decrease MLKL expression in NPC cell (CNE-2 and CR). Trans-well assay was conducted to evaluate invasion. Gene expression profiling was performed using Human U133 2.0 plus arrays (Affymetrix). Kyoto Encyclopedia of Genes and Genomes (KEGG) was adopted to analyze gene expression profiling. Hub genes at a functional level were accessed by protein-to-protein network (PPI). Quantitative real-time PCR and Western blot were used to access EMT markers.ResultsInvasion of CR was about 3~fold change higher than that of CNE-2. Silencing MLKL by siRNA inhibited invasion of CR, not CNE-2. Further, depleting MLKL by CRISPR-Cas9 in CR (CR-MLKL KO) also inhibited its invasion. KEGG pathway analysis showed invasion-related pathways were altered, such as adherent junction, TGF-β signaling pathway. PPI demonstrated that compared with CNE-2, CR showed 9 elevated hub genes including EGFR, JUN, CD44, SPP1, VIM, IL-8, BCL2, WDFY2, PIK3CD and 1 downregulated hub gene CDH1. After MLKL depletion, 8 hub genes were downregulated (EGFR, JUN, CD44, SPP1, VIM, FGF13, PLAU, MMP1) and 2 hub genes were upregulated (MMP9, CDH1). Quantitative real-time PCR results showed that compared with CNE-2, CR displayed decreased epithelial markers significantly (E-Cadherin) and increased mesenchymal markers significantly (Vimentin, N-Cadherin, Zeb1), indicating irradiation-induced EMT. After depletion of MLKL in CR, the expression of E-Cadherin, Vimentin, N-Cadherin, Zeb1 was reversed to the level of CNE-2. Western blot confirmed the results from qRT-PCR.ConclusionsDepletion of MLKL efficiently inhibits invasion of radioresistant NPC by suppressing EMT. MLKL may be an important target to suppress distant metastasis of NPC patients who relapsed after radiotherapy.

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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.

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