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CTHRC1 通过上调 MMP-7/MMP-9 诱导非小细胞肺癌（NSCLC）侵袭。

CTHRC1 induces non-small cell lung cancer (NSCLC) invasion through upregulating MMP-7/MMP-9.

机构信息

Department of Pathology, The First Affiliated Hospital, Sun Yat-sen University, No. 58, ZhongShan Second Road, Guangdong, 510080, China.

Department of Gastrointestinal Surgery, The First Affiliated Hospital, Sun Yat-sen University, No. 58, ZhongShan Second Road, Guangdong, 510080, China.

出版信息

BMC Cancer. 2018 Apr 10;18(1):400. doi: 10.1186/s12885-018-4317-6.

DOI:10.1186/s12885-018-4317-6
PMID:29631554
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5891957/
Abstract

BACKGROUND

The strong invasive and metastatic nature of non-small cell lung cancer (NSCLC) leads to poor prognosis. Collagen triple helix repeat containing 1 (CTHRC1) is involved in cell migration, motility and invasion. The object of this study is to investigate the involvement of CTHRC1 in NSCLC invasion and metastasis.

METHODS

A proteomic analysis was performed to identify the different expression proteins between NSCLC and normal tissues. Cell lines stably express CTHRC1, MMP7, MMP9 were established. Invasion and migration were determined by scratch and transwell assays respectively. Clinical correlations of CTHRC1 in a cohort of 230 NSCLC patients were analysed.

RESULTS

CTHRC1 is overexpressed in NSCLC as measured by proteomic analysis. Additionally, CTHRC1 increases tumour cell migration and invasion in vitro. Furthermore, CTHRC1 expression is significantly correlated with matrix metalloproteinase (MMP)7 and MMP9 expression in sera and tumour tissues from NSCLC. The invasion ability mediated by CTHRC1 were mainly MMP7- and MMP9-dependent. MMP7 or MMP9 depletion significantly eradicated the pro-invasive effects mediated by CTHRC1 on NSCLC cells. Clinically, patients with high CTHRC1 expression had poor survival.

CONCLUSIONS

CTHRC1 serves as a pro-metastatic gene that contributes to NSCLC invasion and metastasis, which are mediated by upregulated MMP7 and MMP9 expression. Targeting CTHRC1 may be beneficial for inhibiting NSCLC metastasis.

摘要

背景

非小细胞肺癌（NSCLC）具有较强的侵袭和转移特性，导致预后不良。胶原蛋白三螺旋重复含 1 型（CTHRC1）参与细胞迁移、运动和侵袭。本研究旨在探讨 CTHRC1 在 NSCLC 侵袭和转移中的作用。

方法

采用蛋白质组学分析鉴定 NSCLC 与正常组织之间差异表达的蛋白。建立稳定表达 CTHRC1、MMP7、MMP9 的细胞系。通过划痕和 Transwell 实验分别测定细胞的侵袭和迁移能力。分析 230 例 NSCLC 患者队列中 CTHRC1 的临床相关性。

结果

蛋白质组学分析表明，CTHRC1 在 NSCLC 中过表达。此外，CTHRC1 增加了体外肿瘤细胞的迁移和侵袭能力。进一步研究发现，CTHRC1 的表达与 NSCLC 患者血清和肿瘤组织中基质金属蛋白酶（MMP）7 和 MMP9 的表达显著相关。CTHRC1 介导的侵袭能力主要依赖于 MMP7 和 MMP9。MMP7 或 MMP9 的耗竭显著消除了 CTHRC1 对 NSCLC 细胞的促侵袭作用。临床研究表明，CTHRC1 高表达的患者生存不良。

结论

CTHRC1 作为一种促转移基因，促进 NSCLC 的侵袭和转移，其机制是通过上调 MMP7 和 MMP9 的表达介导的。靶向 CTHRC1 可能有助于抑制 NSCLC 的转移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c908/5891957/bd1020d38800/12885_2018_4317_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c908/5891957/9b4b7c16436a/12885_2018_4317_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c908/5891957/2bf3639ce5c4/12885_2018_4317_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c908/5891957/c7520cd4c2a2/12885_2018_4317_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c908/5891957/1131e6c2235f/12885_2018_4317_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c908/5891957/ac3e85c31c4f/12885_2018_4317_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c908/5891957/0e5af39cfb72/12885_2018_4317_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c908/5891957/bd1020d38800/12885_2018_4317_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c908/5891957/9b4b7c16436a/12885_2018_4317_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c908/5891957/2bf3639ce5c4/12885_2018_4317_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c908/5891957/c7520cd4c2a2/12885_2018_4317_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c908/5891957/1131e6c2235f/12885_2018_4317_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c908/5891957/ac3e85c31c4f/12885_2018_4317_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c908/5891957/0e5af39cfb72/12885_2018_4317_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c908/5891957/bd1020d38800/12885_2018_4317_Fig7_HTML.jpg

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