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

Authors :
Liantang Wang
Di Xu
Wenting Jiang
Neng Jiang
Yanbin Zhou
Zunfu Ke
Yuefeng Wang
Han Wang
Yu Sun
Hsian-Rong Tseng
Xuenong Zou
Shuhua Li
Yongmei Cui
Zhuo Wang
Yang Zhang
Weiling He
Yangshan Chen
Hui Zhang
Yifeng Luo
Source :
BMC Cancer, Vol 18, Iss 1, Pp 1-14 (2018), BMC Cancer
Publication Year :
2018
Publisher :
Springer Science and Business Media LLC, 2018.

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. Electronic supplementary material The online version of this article (10.1186/s12885-018-4317-6) contains supplementary material, which is available to authorized users.

Details

ISSN :
14712407
Volume :
18
Database :
OpenAIRE
Journal :
BMC Cancer
Accession number :
edsair.doi.dedup.....3081cf34452b2569be48b7fbdfb46ae0