Evidence map›Paper›PMID 25925261›Full record

ArticleBMC cancer2015

FGF9 from cancer-associated fibroblasts is a possible mediator of invasion and anti-apoptosis of gastric cancer cells.

Chao Sun, Hirokazu Fukui, Ken Hara, Xinxing Zhang, Yoshitaka Kitayama, Hirotsugu Eda, Toshihiko Tomita, Tadayuki Oshima, Shojiro Kikuchi, Jiro Watari and 2 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.3field-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

39 citing papers in PubMed, 67 citations in OpenAlex.

  1. FGF family in health and disease.Molecular biomedicine · 2026
    Review
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  3. Article
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  7. Review
  8. FGF9 Recruits β-Catenin to Increase Hepatic ECM Synthesis and Promote NASH-Driven HCC.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Anti-Cancer Effect of Cordycepin on FGF9-Induced Testicular Tumorigenesis.International journal of molecular sciences · 2020
    Article
  17. FGF/FGFR signaling in health and disease.Signal transduction and targeted therapy · 2020
    Review
  18. Interaction of FGF9 with FGFR3-IIIb/IIIc, a putative driver of growth and aggressive behaviour of hepatocellular carcinoma.Liver international : official journal of the International Association for the Study of the Liver · 2020
    Article
  19. Review
  20. Review
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

12 authors at 2 institutions in 2 countries.

Chao SunDivision of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, l-1, Mukogawa, Nishinomiya, 663-8501, Japan. tianjinsunchao@hotmail.com.
Hirokazu FukuiDivision of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, l-1, Mukogawa, Nishinomiya, 663-8501, Japan. hfukui@hyo-med.ac.jp.
Ken HaraDivision of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, l-1, Mukogawa, Nishinomiya, 663-8501, Japan. k-hara@hyo-med.ac.jp.
Xinxing ZhangDivision of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, l-1, Mukogawa, Nishinomiya, 663-8501, Japan. 24167653@qq.com.
Yoshitaka KitayamaDivision of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, l-1, Mukogawa, Nishinomiya, 663-8501, Japan. yoshi-77@hcm-mail.hyo-med.ac.jp.
Hirotsugu EdaDivision of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, l-1, Mukogawa, Nishinomiya, 663-8501, Japan. eda@hyo-med.ac.jp.
Toshihiko TomitaDivision of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, l-1, Mukogawa, Nishinomiya, 663-8501, Japan. tomita@hyo-med.ac.jp.
Tadayuki OshimaDivision of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, l-1, Mukogawa, Nishinomiya, 663-8501, Japan. t-oshima@hyo-med.ac.jp.
Shojiro KikuchiDepartment of Surgery, Hyogo College of Medicine, Nishinomiya, Japan. skikuchi@hyo-med.ac.jp.
Jiro WatariDivision of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, l-1, Mukogawa, Nishinomiya, 663-8501, Japan. watarij@hyo-med.ac.jp.
Mitsuru SasakoDepartment of Surgery, Hyogo College of Medicine, Nishinomiya, Japan. msasako@hyo-med.ac.jp.
Hiroto MiwaDivision of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, l-1, Mukogawa, Nishinomiya, 663-8501, Japan. miwahgi@hyo-med.ac.jp.
Hyogo Medical University · JPTianjin Medical University General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCancer-associated fibroblasts (CAFs), which reside around tumor cells, are suggested to play a pivotal role in tumor progression. Here we performed microarray analyses to compare gene expression profiles between CAFs and non-cancerous gastric fibroblasts (NGFs) from a patient with gastric cancer and found that fibroblast growth factor 9 (FGF9) was a novel growth factor overexpressed in CAFs. We then examined the biological effects of FGF9 during progression of gastric cancer.

methodsExpression of FGF9 in CAFs and NGFs, and their secreted products, were examined by Western blotting. The effects of FGF9 on AGS and MKN28 gastric cancer cells in terms of proliferation, invasion and anti-apoptosis were assessed by WST-1 assay, invasion chamber assay and FACS, respectively. Furthermore, the intracellular signaling by which FGF9 exerts its biological roles was examined in vitro.

resultsFGF9 was strongly expressed in CAFs in comparison with NGFs, being compatible with microarray data indicating that FGF9 was a novel growth factor overexpressed in CAFs. Treatment with FGF9 promoted invasion and anti-apoptosis through activation of the ERK and Akt signaling pathways in AGS and MKN28 cells, whereas these effects were attenuated by treatment with anti-FGF9 neutralizing antibody. In addition, FGF9 treatment significantly enhanced the expression of matrix metalloproteinase 7 (MMP7) in both cell lines.

conclusionsFGF9 is a possible mediator secreted by CAFs that promotes the anti-apoptosis and invasive capability of gastric cancer cells.

Indexed as

Antibodies, NeutralizingApoptosisBiomarkers, TumorCell Line, TumorCell ProliferationFibroblast Growth Factor 9FibroblastsGene Expression Regulation, NeoplasticHumansMAP Kinase Signaling SystemMatrix Metalloproteinase 7Neoplasm InvasivenessSignal TransductionStomach NeoplasmsAntibodies, NeutralizingBiomarkers, TumorFGF9 protein, humanFibroblast Growth Factor 9Matrix Metalloproteinase 7MMP7 protein, human

Identifiers

PMID25925261
PMCPMC4424580
OpenAlexW1984420941

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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.