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ZM336372, a Raf-1 activator, causes suppression of proliferation in a human hepatocellular carcinoma cell line.ZM336372，一种Raf-1激活剂，可抑制人肝癌细胞系的增殖。
J Gastrointest Surg. 2008 May;12(5):852-7. doi: 10.1007/s11605-008-0495-x.
2
Neuroendocrine tumor cell growth inhibition by ZM336372 through alterations in multiple signaling pathways.ZM336372通过多种信号通路的改变抑制神经内分泌肿瘤细胞生长。
Surgery. 2007 Dec;142(6):959-64; discussion 959-64. doi: 10.1016/j.surg.2007.09.020.
3
Inactivation of glycogen synthase kinase-3beta, a downstream target of the raf-1 pathway, is associated with growth suppression in medullary thyroid cancer cells.糖原合酶激酶-3β（raf-1通路的下游靶点）的失活与甲状腺髓样癌细胞的生长抑制有关。
Mol Cancer Ther. 2007 Mar;6(3):1151-8. doi: 10.1158/1535-7163.MCT-06-0665.
4
Glycogen synthase kinase-3--an overview of an over-achieving protein kinase.糖原合酶激酶-3——一种功能多样的蛋白激酶概述
Curr Drug Targets. 2006 Nov;7(11):1377-88. doi: 10.2174/1389450110607011377.
5
Pancreatic cancer: a review of recent advances.胰腺癌：近期进展综述
Expert Opin Investig Drugs. 2006 Nov;15(11):1395-410. doi: 10.1517/13543784.15.11.1395.
6
Aberrant nuclear accumulation of glycogen synthase kinase-3beta in human pancreatic cancer: association with kinase activity and tumor dedifferentiation.糖原合成酶激酶-3β在人胰腺癌中的异常核聚集：与激酶活性和肿瘤去分化的关联
Clin Cancer Res. 2006 Sep 1;12(17):5074-81. doi: 10.1158/1078-0432.CCR-06-0196.
7
Nuclear factor-kappaB in cancer development and progression.核因子-κB在癌症发生发展中的作用
Nature. 2006 May 25;441(7092):431-6. doi: 10.1038/nature04870.
8
ZM336372, a Raf-1 activator, suppresses growth and neuroendocrine hormone levels in carcinoid tumor cells.ZM336372，一种Raf-1激活剂，可抑制类癌肿瘤细胞的生长和神经内分泌激素水平。
Mol Cancer Ther. 2005 Jun;4(6):910-7. doi: 10.1158/1535-7163.MCT-04-0334.
9
Glycogen synthase kinase-3beta participates in nuclear factor kappaB-mediated gene transcription and cell survival in pancreatic cancer cells.糖原合成酶激酶-3β参与胰腺癌细胞核因子κB介导的基因转录和细胞存活过程。
Cancer Res. 2005 Mar 15;65(6):2076-81. doi: 10.1158/0008-5472.CAN-04-3642.
10
Pharmacological inhibitors of glycogen synthase kinase 3.糖原合酶激酶3的药理学抑制剂
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ZM336372 诱导胰腺腺癌细胞系的凋亡与 GSK-3β的磷酸化有关。

ZM336372 induces apoptosis associated with phosphorylation of GSK-3beta in pancreatic adenocarcinoma cell lines.

机构信息

Department of Medicine, University of Wisconsin, Madison, Wisconsin 53792, USA.

出版信息

J Surg Res. 2010 Jun 1;161(1):28-32. doi: 10.1016/j.jss.2009.06.013. Epub 2009 Jul 12.

DOI:10.1016/j.jss.2009.06.013
PMID:20031160
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3379885/
Abstract

INTRODUCTION

ZM336372 is small molecule tyrosine kinase modulator. It has been shown to inhibit glycogen synthase kinase-3beta (GSK-3beta) through phosphorylation of GSK-3beta at Ser 9. GSK-3beta has previously been shown to mediate cell survival in pancreatic cancer cells. Here we determine the effects of ZM336372 on GSK-3beta phosphorylation, apoptosis, and growth in pancreatic adenocarcinoma cell lines.

METHODS

Panc-1 and MiaPaCa-2 cells were treated with ZM336372 or lithium chloride (LiCl) and compared with solvent control. The effects on proliferation for each cell line were determined using the MTT assay. Western blot analysis was performed to examine the effects of treatment on the phosphorylation of GSK-3beta. In addition, western blot was utilized to examine the cleavage of poly (ADP-ribose) polymerase (PARP), a marker of apoptosis.

RESULTS

A dose-dependent increase in phosphorylation of GSK-3beta was observed after treatment with both ZM336372 and LiCl. Growth inhibition due to treatment with ZM336372 and LiCl also occurred in a dose-dependent fashion. An increase in cleaved PARP was demonstrated after treatment with both agents, as was seen previously with GSK-3beta inhibition in pancreatic adenocarcinoma cells.

CONCLUSION

This is the first description of growth inhibition and apoptosis in pancreatic cancer cells related to GSK-3beta inhibition through treatment with ZM336372.

摘要

简介

ZM336372 是一种小分子酪氨酸激酶调节剂。已证实它通过磷酸化 GSK-3β 上的丝氨酸 9 来抑制糖原合酶激酶-3β（GSK-3β）。GSK-3β 先前已被证明可介导胰腺癌细胞的细胞存活。在这里，我们确定 ZM336372 对胰腺腺癌细胞系中 GSK-3β 磷酸化、细胞凋亡和生长的影响。

方法

用 ZM336372 或氯化锂（LiCl）处理 Panc-1 和 MiaPaCa-2 细胞，并与溶剂对照进行比较。用 MTT 测定法确定每种细胞系的增殖效果。进行 Western blot 分析以检查处理对 GSK-3β 磷酸化的影响。此外，还利用 Western blot 检查多聚（ADP-核糖）聚合酶（PARP）的裂解，PARP 是细胞凋亡的标志物。

结果

在用 ZM336372 和 LiCl 处理后，观察到 GSK-3β 的磷酸化呈剂量依赖性增加。ZM336372 和 LiCl 处理引起的生长抑制也呈剂量依赖性。在用两种药物处理后，均证明 cleaved PARP 增加，这与先前在胰腺腺癌细胞中抑制 GSK-3β 时所见的情况相同。

结论

这是首次描述通过用 ZM336372 处理抑制 GSK-3β 导致胰腺癌细胞生长抑制和凋亡。