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首页> 外文期刊>Life sciences >Antimetastatic potential of cardiotoxin III involves inactivation of PI3K/Akt and p38 MAPK signaling pathways in human breast cancer MDA-MB-231 cells
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Antimetastatic potential of cardiotoxin III involves inactivation of PI3K/Akt and p38 MAPK signaling pathways in human breast cancer MDA-MB-231 cells

机译：心脏毒素III的抗转移潜力涉及人乳腺癌MDA-MB-231细胞中PI3K / Akt和p38 MAPK信号通路的失活

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Aim: The aim of this study is to determine whether cardiotoxin III (CTX III) inhibited the metastasis in MDA-MB-231 cells and to further explain its possible mechanisms. Main methods: The MTT assay, wound healing assay, Boyden chamber invasion assay, zymography analysis, reverse transcriptase polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA), inhibitor assay, and Western blot analysis were used to reveal molecular events of CTX III in this study. Key findings: During treatment with non-toxic doses of CTX III, not only cell migration and invasion were markedly suppressed but the expression/activity of matrix metalloproteinase-9 (MMP-9) was also significantly and selectively suppressed in a concentration-dependent manner. In addition, CTX III decreased the nuclear protein level of nuclear factor kappa B (NF-κB), and pretreatment with NF-κB inhibitor (PDTC) or IκB protease inhibitor (TPCK) also reduced MMP-9 expression/activity and cell migration. Our biochemical assays indicated that CTX III potently suppressed the phosphorylation of p38 mitogen-activated protein kinase (MAPK), phosphatidylinositide-3-kinase (PI3K) and Akt. Additionally, the treatment of inhibitors specific for p38 MAPK (SB203580) or PI3K (wortmannin) to cells could result in a reduced expression of NF-κB and MMP-9 expression, concomitantly with an inhibition on cell metastasis. Significance: These results demonstrated that CTX III inhibition of MDA-MB-231 cells may occur through inactivation of both PI3K/Akt and p38 MAPK signaling pathways, exerting inhibitory effects on NF-κB transcriptional factor, thereby decreasing the activity of MMP-9 and then posing an anti-metastatic effect in the cells.
机译：目的：本研究的目的是确定心脏毒素III（CTX III）是否抑制MDA-MB-231细胞中的转移并进一步解释其可能的机制。主要方法：采用MTT测定，伤口愈合测定，Boyden室侵袭测定，酶谱分析，逆转录酶聚合酶链反应（RT-PCR），酶联免疫吸附测定（ELISA），抑制剂测定和Western blot分析来揭示本研究中CTX III的分子事件。主要发现：在用无毒剂量的CTX III治疗期间，不仅细胞迁移和侵袭被显着抑制，而且基质金属蛋白酶9（MMP-9）的表达/活性也被浓度依赖性地显着和选择性地抑制。 。此外，CTX III降低了核因子κB（NF-κB）的核蛋白水平，用NF-κB抑制剂（PDTC）或IκB蛋白酶抑制剂（TPCK）预处理也降低了MMP-9的表达/活性和细胞迁移。我们的生化分析表明，CTX III有效抑制了p38丝裂原激活的蛋白激酶（MAPK），磷脂酰肌醇-3-激酶（PI3K）和Akt的磷酸化。另外，对细胞特异于p38 MAPK（SB203580）或PI3K（渥曼青霉素）的抑制剂的治疗可能导致NF-κB的表达减少和MMP-9的表达减少，同时抑制细胞转移。意义：这些结果表明CTX III对MDA-MB-231细胞的抑制作用可能是通过PI3K / Akt和p38 MAPK信号通路的失活而发生的，从而对NF-κB转录因子产生抑制作用，从而降低了MMP-9和然后在细胞中产生抗转移作用。

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