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首页> 外文期刊>Molecular and Cellular Biology >Persistent Signaling by Dysregulated Thrombin Receptor Trafficking Promotes Breast Carcinoma Cell Invasion
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Persistent Signaling by Dysregulated Thrombin Receptor Trafficking Promotes Breast Carcinoma Cell Invasion

机译：凝血酶受体运输失调的持久信号促进乳腺癌细胞侵袭。

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Increased expression of protease-activated receptor 1 (PAR1), a G protein-coupled receptor for thrombin, has previously been correlated with breast carcinoma cell invasion. PAR1 is irreversibly proteolytically activated, internalized, and sorted directly to lysosomes, a critical process for the termination of signaling. We determined that activated PAR1 trafficking is severely altered in metastatic breast carcinoma cells but not in nonmetastatic or normal breast epithelial cells. Consequently, the proteolytically activated receptor is not sorted to lysosomes and degraded. Altered trafficking of proteolytically activated PAR1 caused sustained activation of phosphoinositide hydrolysis and extracellular signal-regulated kinase signaling, even after thrombin withdrawal, and enhanced cellular invasion. Thus, our results reveal that a novel alteration in trafficking of activated PAR1 causes persistent signaling and, in addition to other processes and proteins, contributes to breast carcinoma cell invasion.
机译：蛋白酶激活受体1（PAR1）是凝血酶的一种G蛋白偶联受体，其表达的增加先前与乳腺癌细胞的侵袭有关。 PAR1被不可逆地蛋白水解激活，内化并直接分类为溶酶体，这是终止信号传导的关键过程。我们确定激活的PAR1转运在转移性乳腺癌细胞中发生了严重变化，但在非转移性或正常的乳腺上皮细胞中则没有变化。因此，蛋白水解激活的受体不被分类为溶酶体并降解。蛋白水解激活的PAR1的改变运输导致磷酸肌醇水解和细胞外信号调节激酶信号传导的持续激活，即使在凝血酶退出后也是如此，并增强了细胞的入侵。因此，我们的结果表明，激活的PAR1转运中的新变化引起持续的信号传导，并且除了其他过程和蛋白质外，还有助于乳腺癌细胞的侵袭。

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