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首页> 外文期刊>Journal of cellular physiology. >Serine peptidase inhibitor Kazal type III (SPINK3) promotes BRL-3A cell proliferation by targeting the PI3K-AKT signaling pathway
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Serine peptidase inhibitor Kazal type III (SPINK3) promotes BRL-3A cell proliferation by targeting the PI3K-AKT signaling pathway

机译：丝氨酸肽酶抑制剂Kazal类型III (SPINK3)针对促进BRL-3A细胞增殖PI3K-AKT信号通路

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摘要

The serine protease inhibitor, Kazal type III (SPINK3), is a trypsin inhibitor associated with liver disease, which highly overexpresses in a variety of cancers. In one of our previous studies of our laboratory, Spink3 was observed to be significantly upregulated in rat liver regeneration (LR) via a gene expression profile. For the current study, rat hepatocyte BRL-3A cells were treated by gene addition/ interference, and the addition of the exogenous rat recombinant protein SPINK3. It was revealed that both the overexpression of endogenous Spink3 and addition of exogenous rat recombinant SPINK3 (rrSPINK3) significantly promoted the cell proliferation of BRL-3A cells, whereas cell proliferation was inhibited when Spink3 was interfered. Furthermore, quantitative reverse transcription polymerase chain reaction and western blot results revealed that three signaling pathways, including extracellular-signal-regulated kinase 1/2 (ERK1/2), Janus kinase (JAK)-signal transducer and activator of transcription (STAT), and phosphatidylinositol-3-kinase (PI3K)-protein kinase B (AKT), as well as their related genes, were altered following endogenous Spink3 addition/interference. Also, the PI3K-AKT and SRC-p38 pathways and their related genes were modified following exogenous SPINK3 treatment. Among them, the common signaling pathway was PI3K-AKT pathway. We concluded that SPINK3 could activate the PI3K-AKT pathway by enhancing the expression of AKT1 to regulate the proliferation of BRL-3A cells. This study may contribute to shedding light on the potential mechanisms of SPINK3 that regulate the proliferation of BRL-3A cells.
机译：丝氨酸蛋白酶抑制剂,Kazal类型III(SPINK3),是一个相关联的胰蛋白酶抑制剂肝脏疾病,高过表达各种各样的癌症。我们实验室的研究,Spink3被观察到在大鼠肝脏显著调节再生(LR)通过基因表达谱。在目前的研究中,老鼠肝细胞BRL-3A细胞治疗基因/干扰和外生的老鼠SPINK3重组蛋白质。这两种内生Spink3的过度和添加外源鼠SPINK3重组(rrSPINK3)显著促进了细胞BRL-3A增殖细胞,而细胞增殖抑制Spink3时干扰。转录聚合酶链反应免疫印迹结果显示,三个信号通路,包括extracellular-signal-regulated激酶1/2(ERK1/2), Janus激酶(激酶)信号传感器和转录激活剂(统计),phosphatidylinositol-3-kinase PI3K蛋白激酶B(一种蛋白激酶),以及相关的基因,内源性Spink3后改变了吗除了/干扰。SRC-p38途径及其相关基因修改后外源性SPINK3治疗。其中,常见的信号通路PI3K-AKT途径。通过增强激活PI3K-AKT途径表达AKT1调节增殖BRL-3A细胞。揭示了潜在的机制SPINK3调节BRL-3A扩散细胞。

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