Evidence map›Paper›PMID 29021002›Full record

ArticleJournal of ovarian research2017

Collagen triple helix repeat containing 1 (CTHRC1) activates Integrin β3/FAK signaling and promotes metastasis in ovarian cancer.

Biying Guo, Huan Yan, Luying Li, Kemin Yin, Fang Ji, Shu Zhang

Open access · goldAbstract read
In one paragraph

Article in Journal of ovarian research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.5field-weighted citation impact, top 11% of its field
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

25 citing papers in PubMed, 39 citations in OpenAlex.

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  15. Model systems for regeneration: the spiny mouse,Development (Cambridge, England) · 2020
    Review
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  17. OncoTargets and therapy · 2020
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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

6 authors at 3 institutions in 1 country.

Biying GuoDepartment of Gynecology and Obstetrics, Shanghai Key Laboratory of Gynecology Oncology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, PuJian Road No.160, Shanghai, 200127, China.
Huan YanDepartment of Gynecology and Obstetrics, Shanghai First Maternity and Infant Hospital, School of Medicine, Shanghai Tong Ji University, Shanghai, 201204, China.
Luying LiDepartment of Gynecology and Obstetrics, Shanghai Key Laboratory of Gynecology Oncology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, PuJian Road No.160, Shanghai, 200127, China.
Kemin YinDepartment of Gynecology and Obstetrics, Shanghai Key Laboratory of Gynecology Oncology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, PuJian Road No.160, Shanghai, 200127, China.
Fang JiDepartment of Gynecology and Obstetrics, Shanghai Key Laboratory of Gynecology Oncology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, PuJian Road No.160, Shanghai, 200127, China. jtj3210@hotmail.com.
Shu ZhangDepartment of Gynecology and Obstetrics, Shanghai Key Laboratory of Gynecology Oncology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, PuJian Road No.160, Shanghai, 200127, China. drzhangshu@126.com.
Shanghai Jiao Tong University · CNRenji Hospital · CNShanghai First Maternity and Infant Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMetastasis is the major cause of morbidity and mortality in patients with epithelial ovarian cancer (EOC), however the mechanisms that underline this process are poorly understood. Collagen triple helix repeat containing-1 (CTHRC1) is a 28-kDa secreted protein reported to be involved in vascular remodeling, bone formation and morphogenesis. This study aimed to investigate the role of CTHRC1 in promoting the metastasis of EOC and to elucidate the underlying molecular mechanisms.

methodsThe biologic functions of CTHRC1 in metastasis were validated both in vivo and in vitro experiments. The phosphor-antibody microarray analysis and Co-immunoprecipitation were performed to detect and identify the integrin β3/FAK signaling pathway that mediated the function of CTHRC1. Seventy two EOC samples were analyzed for association between CTHRC1/integrin β3 expression and patient clinicopathological features.

resultsWe demonstrated that CTHRC1 enhances the biological behavior of EOC including cell migration, invasion, as well as its adhesion capability to cell-extracellular matrix in vitro. Additionally, CTHRC1 promoted metastatic spread of EOC cells in an i.p. ovarian xenograft model and this phenotype was primarily ascribed to the activation of integrin/FAK signaling. Mechanistically, we determined that FAK were phosphorylated on Tyr397, and were activated by integrin β3, which is important for the CTHRC1-mediated migratory and invasive ability of EOC cells in vitro and i.p. metastasis. In addition, we found that attenuated CTHRC1/integrin β3 expression predicted a poor prognostic phenotype and advanced clinical stage of EOC.

conclusionsOur results suggest that CTHRC1, a newly identified regulator of i.p. metastasis through activation of integrin β3/FAK signaling in EOC, may represent a potential therapeutic target for ovarian cancer.

Indexed as

Signal TransductionAdultAgedAnimalsCarcinoma, Ovarian EpithelialCell AdhesionCell Line, TumorCell MovementCell ProliferationDisease Models, AnimalExtracellular Matrix ProteinsFemaleFocal Adhesion Kinase 1HeterograftsHumansIntegrin beta3CTHRC1 protein, humanExtracellular Matrix ProteinsFocal Adhesion Kinase 1Integrin beta3CTHRC1Integrin/FAK signalingMetastasisOvarian cancer

Identifiers

PMID29021002
PMCPMC5637322
OpenAlexW2763380896

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.