一个PSP94-derived PCK3145肽抑制了MMP-9分泌和触发器CD44细胞表面脱落:肿瘤转移的影响。

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Annabi B, Bouzeghrane M,库里JC,霍金斯R, Dulude H, Daigneault L,鲁伊斯M, Wisniewski J,加尔达年代,拉巴尼SA应C,吴JJ,贝力弗R

一个PSP94-derived PCK3145肽抑制了MMP-9分泌和触发器CD44细胞表面脱落:肿瘤转移的影响。

Exp转移。2005;22 (5):429 - 39。

PubMed ID

16283486 (在PubMed

]

文摘

用途:PCK3145合成肽对应于94年前列腺分泌蛋白氨基酸31 - 45岁,这可以减少实验体内骨骼转移和前列腺肿瘤的生长。生物行动的一部分,包括减少循环血浆基质金属蛋白酶9 (MMP),细胞外基质(ECM)降解的关键中介在肿瘤转移和癌细胞的入侵。的antimetastatic PCK3145的作用机制是然而,不理解。实验设计:ht - 1080纤维肉瘤细胞治疗与PCK3145和细胞溶解产物用于免疫印迹分析小GTPase RhoA和膜类型(MT) 1-MMP蛋白质表达。的媒体被用来监控可溶性MMP-9 gelatinolytic活动zymography并通过免疫印迹蛋白质表达。rt - pcr是用来评估RhoA、MT1-MMP MMP-9,顾虑和CD44基因表达。流式细胞仪是用于监测细胞表面表达CD44和膜结合MMP-9。细胞粘附进行不同纯化ECM蛋白质,当细胞迁移特别透明质酸(HA)上执行。结果:我们发现PCK3145抑制ht - 1080细胞粘附到哈,laminin-1, i型胶原暗示的共同影响细胞表面受体CD44。事实上,PCK3145触发CD44的脱落细胞表面的媒体。 PCK3145 also inhibited MMP-9 secretion and binding to the cell surface. This effect was correlated to increased RhoA and MT1-MMP gene and protein expression. CONCLUSIONS: Our data suggest that PCK3145 may antagonize tumor cell metastatic processes by inhibiting both MMP-9 secretion and its potential binding to its cell surface docking receptor CD44. Such mechanism may involve RhoA signaling and increase in MT1-MMP-mediated CD44 shedding. Together with its beneficial effects in clinical trials, this is the first demonstration of PCK3145 acting as a MMP secretion inhibitor.

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