Evidence map›Paper›PMID 28600569›Full record

ArticleScientific reports2017

FPR2 promotes invasion and metastasis of gastric cancer cells and predicts the prognosis of patients.

Xi-Lu Hou, Cheng-Dong Ji, Jun Tang, Yan-Xia Wang, Dong-Fang Xiang, Hai-Qing Li, Wei-Wei Liu, Jiao-Xue Wang, He-Zhong Yan, Yan Wang and 5 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

32 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Formyl Peptide Receptor-2-Suppressed Autophagy Promotes the Migration and Invasion of Human Glioblastoma Cells Through PI3K/Akt Signaling.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Article
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  5. The role and application prospects of ANXA1 in gastric cancer cells.Medical oncology (Northwood, London, England) · 2025
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  12. WKYMVm Works by Targeting Immune Cells.Journal of inflammation research · 2023
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  15. Review
  16. Therapeutic potential of WKYMVm in diseases.Frontiers in pharmacology · 2022
    Review
  17. Caulerpin MitigatesInternational journal of molecular sciences · 2021
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  18. 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

15 authors at 3 institutions in 2 countries.

Xi-Lu HouDepartment of Gastroenterology, The 105th Hospital of People's Liberation Army, Hefei, Anhui, 230031, China.
Cheng-Dong JiInstitute of Pathology & Southwest Cancer Center, and Key Laboratory of Tumor Immunopathology, Ministry of Education of China, Third Military Medical University, Chongqing, 400038, China.
Jun TangDepartment of Gastroenterology, The 105th Hospital of People's Liberation Army, Hefei, Anhui, 230031, China.
Yan-Xia WangInstitute of Pathology & Southwest Cancer Center, and Key Laboratory of Tumor Immunopathology, Ministry of Education of China, Third Military Medical University, Chongqing, 400038, China.
Dong-Fang XiangInstitute of Pathology & Southwest Cancer Center, and Key Laboratory of Tumor Immunopathology, Ministry of Education of China, Third Military Medical University, Chongqing, 400038, China.
Hai-Qing LiDepartment of Gastroenterology, The 105th Hospital of People's Liberation Army, Hefei, Anhui, 230031, China.
Wei-Wei LiuDepartment of Gastroenterology, The 105th Hospital of People's Liberation Army, Hefei, Anhui, 230031, China.
Jiao-Xue WangDepartment of Gastroenterology, The 105th Hospital of People's Liberation Army, Hefei, Anhui, 230031, China.
He-Zhong YanDepartment of Gastroenterology, The 105th Hospital of People's Liberation Army, Hefei, Anhui, 230031, China.
Yan WangInstitute of Pathology & Southwest Cancer Center, and Key Laboratory of Tumor Immunopathology, Ministry of Education of China, Third Military Medical University, Chongqing, 400038, China.
Peng ZhangInstitute of Pathology & Southwest Cancer Center, and Key Laboratory of Tumor Immunopathology, Ministry of Education of China, Third Military Medical University, Chongqing, 400038, China.
You-Hong CuiInstitute of Pathology & Southwest Cancer Center, and Key Laboratory of Tumor Immunopathology, Ministry of Education of China, Third Military Medical University, Chongqing, 400038, China.
Ji-Ming WangLaboratory of Molecular Immunoregulation, Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, Frederick, MD, 21702, USA.
Xiu-Wu BianInstitute of Pathology & Southwest Cancer Center, and Key Laboratory of Tumor Immunopathology, Ministry of Education of China, Third Military Medical University, Chongqing, 400038, China. bianxiuwu@263.net.
Wei LiuDepartment of Gastroenterology, The 105th Hospital of People's Liberation Army, Hefei, Anhui, 230031, China. weiliu105@126.com.
117th Hospital of People's Liberation Army · CNArmy Medical University · CNNational Cancer Institute · US

Funding

The Role of Cellular Receptors Involved in Inflammation and Tumor ProgressionZIABC010015 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WANG, JI MING · 2009 to 2023
$6.3M
6 · The paper itself

Abstract

Formyl peptide receptor 2 (FPR2), a classical chemoattractant receptor of G-protein-coupled receptors, is reported to be involved in invasion and metastasis of some cancers, but the role of FPR2 in gastric cancer (GC) has not yet been elucidated. In this study, we found that the levels of FPR2 expression in GC were positively correlated with invasion depth, lymph node metastasis and negatively correlated with the patients' overall survival. Multivariate analysis indicated that FPR2 expression was an independent prognostic marker for GC patients. FPR2-knockdown significantly abrogated the migration and invasion stimulated by Hp(2-20) and Ac(2-26), two well-characterized ligands for FPR2 in GC cells. FPR2 deletion also reduced the tumorigenic and metastatic capabilities of GC cells in vivo. Mechanistically, stimulation with FPR2 ligands resulted in down-regulation of E-cadherin and up-regulation of vimentin, which were reversed by FPR2 knock-down, implying the involvement of epithelial-mesenchymal transition (EMT). Moreover, the activation of FPR2 was accompanied with ERK1/2 phosphorylation, which could be attenuated by FPR2 silencing or treatment with MEK inhibitor, PD98059. Altogether, our results demonstrate that FPR2 is functionally involved in invasion and metastasis, and potentially acts as a novel prognostic marker as well as a potential therapeutic target in human GC.

Indexed as

Gene Expression Regulation, NeoplasticAgedAnimalsAntigens, CDBiomarkers, TumorCadherinsCell Line, TumorEpithelial-Mesenchymal TransitionFemaleHumansLymphatic MetastasisMaleMiceMice, NudeMiddle AgedMitogen-Activated Protein Kinase 1Antigens, CDBiomarkers, TumorCadherinsCDH1 protein, humanFPR2 protein, humanMAPK1 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Receptors, Formyl PeptideReceptors, LipoxinRNA, Small InterferingVimentin

Identifiers

PMID28600569
PMCPMC5466646
OpenAlexW2622117301

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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.