Evidence map›Paper›PMID 29631554›Full record

ArticleBMC cancer2018

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

Weiling He, Hui Zhang, Yuefeng Wang, Yanbin Zhou, Yifeng Luo, Yongmei Cui, Neng Jiang, Wenting Jiang, Han Wang, Di Xu and 9 more

Abstract read
In one paragraph

Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

48 citing papers in PubMed.

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  11. Tankyrase 2 promotes lung cancer cell malignancy.World journal of clinical oncology · 2024
    Article
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  15. The Effect ofBioMed research international · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

19 authors.

Weiling HeDepartment of Pathology, The First Affiliated Hospital, Sun Yat-sen University, No. 58, ZhongShan Second Road, Guangdong, 510080, China.
Hui ZhangDepartment of Pathology, The First Affiliated Hospital, Sun Yat-sen University, No. 58, ZhongShan Second Road, Guangdong, 510080, China.
Yuefeng WangDepartment of Pathology, The First Affiliated Hospital, Sun Yat-sen University, No. 58, ZhongShan Second Road, Guangdong, 510080, China.
Yanbin ZhouDepartment of Respiratory Medicine, The First Affiliated Hospital, Sun Yat-sen University, No. 58, ZhongShan Second Road, Guangdong, 510080, China.
Yifeng LuoDepartment of Respiratory Medicine, The First Affiliated Hospital, Sun Yat-sen University, No. 58, ZhongShan Second Road, Guangdong, 510080, China.
Yongmei CuiDepartment of Pathology, The First Affiliated Hospital, Sun Yat-sen University, No. 58, ZhongShan Second Road, Guangdong, 510080, China.
Neng JiangDepartment of Pathology, The First Affiliated Hospital, Sun Yat-sen University, No. 58, ZhongShan Second Road, Guangdong, 510080, China.
Wenting JiangDepartment of Pathology, The First Affiliated Hospital, Sun Yat-sen University, No. 58, ZhongShan Second Road, Guangdong, 510080, China.
Han WangDepartment of Pathology, The First Affiliated Hospital, Sun Yat-sen University, No. 58, ZhongShan Second Road, Guangdong, 510080, China.
Di XuDepartment of Thoracic Surgery, The Central Hospital of Wuhan, No.26 Shenli Street, Jiang'an District, Wuhan, 430014, Hubei Province, China.
Shuhua LiDepartment of Pathology, The First Affiliated Hospital, Sun Yat-sen University, No. 58, ZhongShan Second Road, Guangdong, 510080, China.
Zhuo WangDepartment of Pathology, The First Affiliated Hospital, Sun Yat-sen University, No. 58, ZhongShan Second Road, Guangdong, 510080, China.
Yangshan ChenDepartment of Pathology, The First Affiliated Hospital, Sun Yat-sen University, No. 58, ZhongShan Second Road, Guangdong, 510080, China.
Yu SunDepartment of Pathology, The First Affiliated Hospital, Sun Yat-sen University, No. 58, ZhongShan Second Road, Guangdong, 510080, China.
Yang ZhangBiomedical Engineering, The University of Texas at El Paso, El Paso, TX, USA.
Hsian-Rong TsengDepartment of Molecular and Medical Pharmacology, Crump Institute for Molecular Imaging (CIMI), California NanoSystems Institute (CNSI), University of California, Los Angeles, 570 Westwood Plaza, California, Los Angeles, 90095-1770, USA.
Xuenong ZouGuangdong Provincial Key Laboratory of Orthopedics and Traumatology, The First Affiliated Hospital, Sun Yat-sen University, No. 58, ZhongShan Second Road, Guangdong, 510080, China.
Liantang WangDepartment of Pathology, The First Affiliated Hospital, Sun Yat-sen University, No. 58, ZhongShan Second Road, Guangdong, 510080, China.
Zunfu KeDepartment of Pathology, The First Affiliated Hospital, Sun Yat-sen University, No. 58, ZhongShan Second Road, Guangdong, 510080, China. kezunfu@mail.sysu.edu.cn.

Funding

Guangzhou Science and Technology Planning Program 2014J4100132Guangzhou Science and Technology Planning Program 2015A020214010National Natural Science Foundation of China 30900650National Natural Science Foundation of China 81372501Natural Science Foundation of Guangdong Province 2011B031800025Natural Science Foundation of Guangdong Province S2012010008378
6 · The paper itself

Abstract

backgroundThe 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.

methodsA 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.

resultsCTHRC1 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.

conclusionsCTHRC1 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.

Indexed as

Gene Expression Regulation, NeoplasticCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementCell ProliferationExtracellular Matrix ProteinsFemaleHumansImmunohistochemistryLung NeoplasmsMaleMatrix Metalloproteinase 7Matrix Metalloproteinase 9NF-kappa BPrognosisPromoter Regions, GeneticCTHRC1 protein, humanExtracellular Matrix ProteinsMatrix Metalloproteinase 7Matrix Metalloproteinase 9NF-kappa BProto-Oncogene Proteins c-junCTHRC1Invasion/metastasisLung cancerMMP7MMP9

Identifiers

PMID29631554
PMCPMC5891957

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.