Evidence map›Paper›PMID 28716029›Full record

ArticleMolecular cancer2017

FOXP3 promotes tumor growth and metastasis by activating Wnt/β-catenin signaling pathway and EMT in non-small cell lung cancer.

Shucai Yang, Yi Liu, Ming-Yue Li, Calvin S H Ng, Sheng-Li Yang, Shanshan Wang, Chang Zou, Yujuan Dong, Jing Du, Xiang Long and 5 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 284 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
284citing papers in PubMed, 3 pooled it
10.4field-weighted citation impact, top 1% 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

284 citing papers in PubMed, 3 syntheses or guidelines pooled it, 421 citations in OpenAlex.

  1. Pooled it
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  14. Foxp3Current gene therapy · 2026
    Article
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224 more citing papers are in PubMed but not listed here.

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

15 authors at 6 institutions in 1 country.

Shucai YangDepartment of Clinical Laboratory, Pingshan District People's Hospital Of Shenzhen, Shenzhen, China.
Yi LiuDepartment of Surgery, the Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, NT, Hong Kong, China.
Ming-Yue LiDepartment of Surgery, the Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, NT, Hong Kong, China.
Calvin S H NgDepartment of Surgery, the Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, NT, Hong Kong, China.
Sheng-Li YangDepartment of Surgery, the Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, NT, Hong Kong, China.
Shanshan WangDepartment of Otorhinolaryngology, Head and Neck Surgery, the Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, NT, Hong Kong, China.
Chang ZouClinical Research Centre, Shenzhen People's Hospital, the Second Clinical Medical College of Jinan University, Shenzhen, China.
Yujuan DongDepartment of Surgery, the Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, NT, Hong Kong, China.
Jing DuPeking University Shenzhen Hospital, Shenzhen, Guangdong, China.
Xiang LongPeking University Shenzhen Hospital, Shenzhen, Guangdong, China.
Li-Zhong LiuFaculty of Medicine, Shenzhen University Health Science Center, Shenzhen University, Shenzhen, China.
Innes Y P WanDepartment of Surgery, the Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, NT, Hong Kong, China.
Tony MokDepartment of Clinical Oncology, the Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, NT, Hong Kong, China.
Malcolm J UnderwoodDepartment of Surgery, the Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, NT, Hong Kong, China.
George G ChenDepartment of Surgery, the Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, NT, Hong Kong, China. gchen@cuhk.edu.hk.
Chinese University of Hong Kong · CNPrince of Wales Hospital · CNPeking University Shenzhen Hospital · CNChinese University of Hong Kong, Shenzhen · CNJinan University · CNShenzhen University Health Science Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe role of cancer cell FOXP3 in tumorigenesis is conflicting. We aimed to study FOXP3 expression and regulation, function and clinical implication in human non-small cell lung cancer (NSCLC).

methodsOne hundred and six patients with histologically-confirmed NSCLC who underwent surgery were recruited for the study. Tumor samples and NSCLC cell lines were used to examine FOXP3 and its related molecules. Various cell functions related to tumorigenesis were performed. In vivo mouse tumor xenograft was used to confirm the in vitro results.

resultsNSCLC patients with the high level of FOXP3 had a significant decrease in overall survival and recurrence-free survival. FOXP3 overexpression significantly induced cell proliferation, migration, and invasion, whereas its inhibition impaired its oncogenic function. In vivo studies confirmed that FOXP3 promoted tumor growth and metastasis. The ectopic expression of FOXP3 induced epithelial-mesenchymal transition (EMT) with downregulation of E-cadherin and upregulation of N-cadherin, vimentin, snail, slug, and MMP9. The oncogenic effects by FOXP3 could be attributed to FOX3-mediated activation of Wnt/β-catenin signaling, as FOXP3 increased luciferase activity of Topflash reporter and upregulated Wnt signaling target genes including c-Myc and Cyclin D1 in NSCLC cells. Co-immunoprecipitation results further indicated that FOXP3 could physically interacted with β-catenin and TCF4 to enhance the functions of β-catenin and TCF4, inducing transcription of Wnt target genes to promote cell proliferation, invasion and EMT induction.

conclusionsFOXP3 can act as a co-activator to facilitate the Wnt-b-catenin signaling pathway, inducing EMT and tumor growth and metastasis in NSCLC.

Indexed as

Epithelial-Mesenchymal TransitionWnt Signaling PathwayAnimalsCarcinogenesisCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationForkhead Transcription FactorsHEK293 CellsHumansLung NeoplasmsMice, NudeNeoplasm MetastasisPrognosisForkhead Transcription FactorsFOXP3 protein, humanEMTFOXP3NSCLCTCF4Wnt

Identifiers

PMID28716029
PMCPMC5514503
OpenAlexW2735265951

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.