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首页> 外文期刊>Molecular and Cellular Biochemistry: An International Journal for Chemical Biology >Acacetin, a flavonoid, inhibits the invasion and migration of human prostate cancer DU145 cells via inactivation of the p38 MAPK signaling pathway.
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Acacetin, a flavonoid, inhibits the invasion and migration of human prostate cancer DU145 cells via inactivation of the p38 MAPK signaling pathway.

机译：Acacetin，一种类黄酮，抑制人前列腺癌DU145细胞通过灭活P38 MAPK信号通路的侵袭和迁移。

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摘要

Acacetin (5,7-dihydroxy-4'-methoxyflavone), a flavonoid compound, has anti-peroxidative and anti-inflammatory effects. The effect of acacetin on antimetastasis in human prostate cancer DU-145 cells was investigated. First, the result demonstrated acacetin could exhibit an inhibitory effect on the abilities of the adhesion, invasion, and migration by cell-matrix adhesion assay, wound-healing assay, and Boyden chamber assay. Data also showed acacetin could inhibit the phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) involved in the downregulation of the expressions of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), and urokinase-type plasminogen activator (u-PA) at both the protein and mRNA levels. Next, acacetin significantly decreased the nuclear levels of nuclear factor kappa B (NF-kappaB), c-Fos, and c-Jun. Also, the treatment with acacetin to DU145 cells also leads to a dose-dependent inhibition on the binding ability of NF-kappaB and activator protein-1 (AP-1). Furthermore, the treatment of inhibitors specific for p38 MAPK (SB203580) to DU145 cells could cause reduced expressions of MMP-2, MMP-9, and u-PA. These results showed acacetin could inhibit the invasion and migration abilities of DU145 cells by reducing MMP-2, MMP-9, and u-PA expressions through suppressing p38 MAPK signaling pathway and inhibiting NF-kappaB- or AP-1-binding activity. These findings proved acacetin might be offered further application as an antimetastatic agent.
机译：Acacetin（5,7-二羟基-4'-甲氧基氟），一种类黄酮化合物，具有抗过氧化和抗炎作用。研究了对人前列腺癌DU-145细胞中抗体糖的影响。首先，结果证明了Acacetin可以表现出对粘合，侵袭和迁移的能力的抑制作用，通过细胞基质粘附测定，伤口愈合测定和Boyden室测定。数据也显示Acacetin可以抑制P38丝裂原激活的蛋白激酶（P38Mapk）的磷酸化参与基质金属蛋白酶-2（MMP-2），基质金属蛋白酶-9（MMP-9）和尿激酶 - 尿激酶的下调在蛋白质和mRNA水平的型纤溶酶原激活剂（U-PA）。接下来，Acacetin显着降低了核因子Kappa B（NF-κB），C-FOS和C-Jun的核水平。此外，用Acacetin至Du145细胞的处理也导致对NF-Kappab和活化剂蛋白-1（AP-1）的结合能力的剂量依赖性抑制。此外，对P38MapK（SB203580）的抑制剂的治疗可引起MMP-2，MMP-9和U-PA的减少表达。这些结果表明，通过抑制P38 MAPK信号通路并抑制NF-κB或AP-1结合活性，通过减少MMP-2，MMP-9和U-PA表达来抑制DU145细胞的侵袭和迁移能力。这些结果证明，可以将Acacetin进一步申请为抗使剂。

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