Evidence map›Paper›PMID 34427817›Full record

ArticleDigestive diseases and sciences2022

Overexpression of FOXC1 Promotes Tumor Metastasis by Activating the Wnt/β-Catenin Signaling Pathway in Gastric Cancer.

Yang'an Sun, Chao Lin, Qunhua Ding, Ying Dai

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In one paragraph

Article in Digestive diseases and sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

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  6. Review
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  8. Wnt/β-catenin-driven EMT regulation in human cancers.Cellular and molecular life sciences : CMLS · 2024
    Review
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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

4 authors at 2 institutions in 1 country.

Yang'an SunAbdominal Surgery Department, Affiliated Tumor Hospital of Nanchang University, Jiangxi Tumor Hospital, Nanchang, Jiangxi, China.
Chao LinAbdominal Surgery Department, Affiliated Tumor Hospital of Nanchang University, Jiangxi Tumor Hospital, Nanchang, Jiangxi, China.
Qunhua DingAbdominal Surgery Department, Affiliated Tumor Hospital of Nanchang University, Jiangxi Tumor Hospital, Nanchang, Jiangxi, China.
Ying DaiThe Third Hepatology Department, Nanchang No. 9 Hospital, Nanchang Liverish Hospital, 167 Hongdu Middle Ave, Qingshanhu District, Nanchang, 330002, Jiangxi, China. daiying783@gmail.com.ORCID 0000-0003-1787-6060
Nanchang University · CNThird Hospital of Nanchang · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundForkhead box protein C1 (FOXC1) is a transcription factor overexpressed in multiple cancers and is associated with poor prognosis. However, the function of FOXC1 in gastric cancer remains largely unknown.

aimThis study aims to explore the role of FOXC1 in promoting gastric cancer metastasis.

methodsFOXC1 expression in gastric cancer patients was measured using real-time PCR and western blot. The association of FOXC1 with patient survival was assessed using public dataset. Gastric cancer cells with FOXC1 overexpression or knockdown were established. Cell metastatic ability was assessed by the expression of epithelial-mesenchymal transition (EMT)-related genes (E-cadherin, N-cadherin, vimentin) and matrix metalloproteinase-9 (MMP-9) as well as by migration and invasion assays. Chromatin immunoprecipitation was used to evaluate the interaction between FOXC1 and β-catenin. The in vivo effect of FOXC1 and β-catenin was assessed in metastatic animal models.

resultsFOXC1 is overexpressed in gastric cancer and is associated with disease progression and poor patient survival. FOXC1 overexpression leads to the down-regulation of epithelial marker (E-cadherin) and the up-regulation of mesenchymal makers (N-cadherin, vimentin) and MMP-9, consistent with enhanced EMT. Moreover, cell migration and invasion are also activated, indicating increased metastatic ability. Notably, FOXC1 binds to the promoter region of β-catenin and transactivates β-catenin expression, which is responsible for the activation of EMT and metastasis in cells overexpressing FOXC1, while β-catenin knockdown can suppress the metastasis-induced by FOXC1.

conclusionsFOXC1 promotes gastric cancer metastasis by activating Wnt/β-catenin signaling pathway, which may serve as a promising therapeutic target for gastric cancer treatment.

Indexed as

Stomach NeoplasmsWnt Signaling PathwayAnimalsbeta CateninCadherinsCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticMatrix Metalloproteinase 9Vimentinbeta CateninCadherinsMatrix Metalloproteinase 9VimentinEpithelial–mesenchymal transition (EMT)Forkhead box protein C1 (FOXC1)Gastric cancerMetastasisWnt/β-catenin signaling pathway

Identifiers

PMID34427817
OpenAlexW3194327487

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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.