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表皮生长因子受体的脂筏定位通过MAPK/ERK信号通路改变SiHa细胞中基质金属蛋白酶-1的表达。

Lipid raft localization of epidermal growth factor receptor alters matrix metalloproteinase-1 expression in SiHa cells via the MAPK/ERK signaling pathway.

作者信息

Zhang Zongfeng, Wang Lina, Du Juan, Li Yuanbo, Yang Huilun, Li Chenxi, Li Hui, Hu Haiyang

机构信息

Department of Obstetrics and Gynecology, Second Affiliated Hospital, Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China.

出版信息

Oncol Lett. 2016 Dec;12(6):4991-4998. doi: 10.3892/ol.2016.5307. Epub 2016 Oct 24.

DOI:10.3892/ol.2016.5307
PMID:28101233
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5228301/
Abstract

Matrix metalloproteinase-1 (MMP-1) has been identified as an important participant in tumor invasion, metastasis and angiogenesis. The purpose of the present study was to investigate the effects of epidermal growth factor receptor (EGFR) localization to lipid rafts on signaling pathways involved in the regulation of MMP-1 expression in SiHa cells, a cervical cancer cell line. EGFR activation by EGF specifically induced MMP-1 expression at both the messenger RNA and protein levels. Additionally, it was observed that EGFR localized to lipid rafts, and that the redistribution of EGFR induced by lipid raft disruption strengthened EGF-induced MMP-1 expression. MMP-1 induction was blocked by the mitogen-activated protein kinase (MAPK) kinase inhibitors PD98059 and U0126. Our results suggested that lipid rafts provide a platform to inhibit EGFR regulation of MMP-1 in SiHa cells through the MAPK/extracellular signal-regulated kinase signaling pathway.

摘要

基质金属蛋白酶-1（MMP-1）已被确定为肿瘤侵袭、转移和血管生成的重要参与者。本研究的目的是探讨表皮生长因子受体（EGFR）定位于脂筏对参与调控人宫颈癌SiHa细胞系中MMP-1表达的信号通路的影响。表皮生长因子（EGF）激活EGFR可在信使核糖核酸和蛋白质水平上特异性诱导MMP-1表达。此外，观察到EGFR定位于脂筏，脂筏破坏诱导的EGFR重新分布增强了EGF诱导的MMP-1表达。丝裂原活化蛋白激酶（MAPK）激酶抑制剂PD98059和U0126可阻断MMP-1的诱导。我们的结果表明，脂筏提供了一个平台，通过MAPK/细胞外信号调节激酶信号通路抑制SiHa细胞中EGFR对MMP-1的调控。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8777/5228301/5e925561e8f5/ol-12-06-4991-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8777/5228301/42b75572f7ef/ol-12-06-4991-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8777/5228301/65ef541225aa/ol-12-06-4991-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8777/5228301/f6d2edebeae0/ol-12-06-4991-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8777/5228301/5e925561e8f5/ol-12-06-4991-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8777/5228301/42b75572f7ef/ol-12-06-4991-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8777/5228301/65ef541225aa/ol-12-06-4991-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8777/5228301/f6d2edebeae0/ol-12-06-4991-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8777/5228301/5e925561e8f5/ol-12-06-4991-g03.jpg

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