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首页> 外文期刊>Trends in Ecology & Evolution >Pomegranate extract inhibits migration and invasion of oral cancer cells by downregulating matrix metalloproteinase-2/9 and epithelial-mesenchymal transition
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Pomegranate extract inhibits migration and invasion of oral cancer cells by downregulating matrix metalloproteinase-2/9 and epithelial-mesenchymal transition

机译：石榴提取物通过下调基质金属蛋白酶-2 / 9和上皮间充质转换来抑制口腔癌细胞的迁移和侵袭

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Discovering drug candidates for the modulation of metastasis is of great importance in inhibiting oral cancer malignancy. Although most pomegranate extract applications aim at the antiproliferation of cancer cells, its antimetastatic effects remain unclear, especially for oral cancer cells. The aim of this study is to evaluate the change of two main metastasis characters, migration and invasion of oral cancer cells. Further, we want to explore the molecular mechanisms of action of pomegranate extract (POMx) at low cytotoxic concentration. We found that POMx ranged from 0 to 50 mu g/mL showing low cytotoxicity to oral cancer cells. In the case of oral cancer HSC-3 and Ca9-22 cells, POMx inhibits wound healing migration, transwell migration, and matrix gel invasion. Mechanistically, POMx downregulates matrix metalloproteinase (MMP)-2 and MMP-9 activities and expressions as well as epithelial-mesenchymal transition (EMT) signaling. POMx upregulates extracellular signal-regulated kinases 1/2 (ERK1/2), but not c-Jun N-terminal kinase (JNK) and p38 expression. Addition of ERK1/2 inhibitor (PD98059) significantly recovered the POMx-suppressed transwell migration and MMP-2/-9 activities in HSC-3 cells. Taken together, these findings suggest to further test low cytotoxic concentrations of POMx as a potential antimetastatic therapy against oral cancer cells.
机译：发现转移调节的药物候选者在抑制口腔癌症恶性肿瘤方面具有重要意义。虽然大多数石榴提取物应用旨在瞄准癌细胞的抗溶解，但其抗致动效应仍然不清楚，特别是对于口服癌细胞。本研究的目的是评估两种主要转移性状，迁移和口腔癌细胞的侵袭的变化。此外，我们希望在低细胞毒性浓度下探讨石榴提取物（POMX）的作用的分子机制。我们发现POMX从0到50μg/ ml显示出对口服癌细胞的低细胞毒性。在口腔癌HSC-3和CA9-22细胞的情况下，POMX抑制伤口愈合迁移，Transwell迁移和基质凝胶侵袭。机械地，POMX下调基质金属蛋白酶（MMP）-2和MMP-9和表达以及上皮 - 间充质转换（EMT）信号传导。 POMX上调细胞外信号调节激酶1/2（ERK1 / 2），但不是C-JUN N-末端激酶（JNK）和P38表达。添加ERK1 / 2抑制剂（PD98059）显着回收了HSC-3细胞中的POMx抑制的Transwell迁移和MMP-2 / -9活性。这些发现结合在一起，表明，进一步测试低细胞毒性浓度的POMX作为对口腔癌细胞的潜在抗致抗体治疗。

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