激肽释放酶相关肽酶信号在结肠癌细胞中的作用：靶向蛋白酶激活受体。
Kallikrein-related peptidase signaling in colon carcinoma cells: targeting proteinase-activated receptors.
机构信息
Department of Physiology and Pharmacology, University of Calgary, AB, Canada.
出版信息
Biol Chem. 2012 Apr;393(5):413-20. doi: 10.1515/bc-2011-231.
We hypothesized that kallikrein-related peptidase 14 (KLK14) is produced by colonic tumors and can promote tumorigenesis by activating proteinase-activated receptors (PARs). We found that KLK14 is expressed in human colon adenocarcinoma cells but not in adjacent cancer-free tissue; KLK14 mRNA, present in colon cancer, leads to KLK14 protein expression and secretion; and KLK14 signals viaPAR-2 in HT-29 cells to cause (1) receptor activation/internalization, (2) increases in intracellular calcium, (3) stimulation of ERK1/2/MAP kinase phosphorylation, and (4) cell proliferation. We suggest that KLK14, acting via PAR-2, represents an autocrine/paracrine regulator of colon tumorigenesis.
我们假设激肽释放酶相关肽酶 14（KLK14）由结肠肿瘤产生，并通过激活蛋白酶激活受体（PAR）促进肿瘤发生。我们发现 KLK14 在人结肠腺癌细胞中表达，但在相邻无癌组织中不表达；存在于结肠癌中的 KLK14 mRNA 导致 KLK14 蛋白表达和分泌；KLK14 通过 HT-29 细胞中的 PAR-2 信号转导引起（1）受体激活/内化，（2）细胞内钙离子增加，（3）ERK1/2/MAP 激酶磷酸化的刺激，以及（4）细胞增殖。我们认为，通过 PAR-2 起作用的 KLK14 代表结肠肿瘤发生的自分泌/旁分泌调节剂。
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