ArticleOncogene2019
FGF18, a prominent player in FGF signaling, promotes gastric tumorigenesis through autocrine manner and is negatively regulated by miR-590-5p.
Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 59 citations in OpenAlex.
- FGF18 mediates fibroblast-leukemia cross talk to promote acute myeloid leukemia progression.Blood · 2026Article
- The interaction between inflammation and estrogen in adenomyosis : from molecular mechanisms to therapeutic strategies.Seminars in immunopathology · 2026Review
- Wilms Tumor 1-Expressing Stromal Cells Promote Pancreatic Cancer Progression.Cancer research · 2026Article
- Transgenerational inheritance of diminished ovarian reserve triggered by prenatal propylparaben exposure in mice.Nature communications · 2025Article
- Implications of miRNA-590 dysregulation in digestive tract malignancies: mechanistic aspects and clinical significance.Molecular biology reports · 2025Review
- High FGF18 expression levels predict poor prognosis in endometrial carcinoma patients and promote tumor growth and metastasis.The Journal of international medical research · 2025Article
- Roles of fibroblast growth factors in the treatment of diabetes.World journal of diabetes · 2024Review
- Article
- miR-590-5p/Tiam1-mediated glucose metabolism promotes malignant evolution of pancreatic cancer by regulating SLC2A3 stability.Cancer cell international · 2023Article
- Gastric Cancer: Molecular Mechanisms, Novel Targets, and Immunotherapies: From Bench to Clinical Therapeutics.Cancers · 2023Review
- Fibroblast growth factor 18 stimulates the proliferation of hepatic stellate cells, thereby inducing liver fibrosis.Nature communications · 2023Article
- Circulating FGF18 is decreased in pleural mesothelioma but not correlated with disease prognosis.Thoracic cancer · 2023Article
- Biological and clinical implications of FGFR aberrations in paediatric and young adult cancers.Oncogene · 2023Review
- Exploring the Structural and Functional Diversity among FGF Signals: A Comparative Study of Human, Mouse, and Xenopus FGF Ligands in Embryonic Development and Cancer Pathogenesis.International journal of molecular sciences · 2023Review
- The role of fibroblast growth factor 18 in cancers: functions and signaling pathways.Frontiers in oncology · 2023Review
- Signaling pathways and therapeutic interventions in gastric cancer.Signal transduction and targeted therapy · 2022Review
- Small RNA-Seq Reveals Similar miRNA Transcriptome in Children and Young Adults with T-ALL and Indicates miR-143-3p as Novel Candidate Tumor Suppressor in This Leukemia.International journal of molecular sciences · 2022Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- HSP90-CDC37 functions as a chaperone for the oncogenic FGFR3-TACC3 fusion.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- HDAC7 promotes NSCLC proliferation and metastasis via stabilization by deubiquitinase USP10 and activation of β-catenin-FGF18 pathway.Journal of experimental & clinical cancer research : CR · 2022Article
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 2 countries.
Funding
Abstract
Fibroblast growth factors (FGFs) and their receptors are significant components during fundamental cellular processes. FGF18 plays a distinctive role in modulating the activity of both tumor cells and tumor microenvironment. This study aims to comprehensively investigate the expression and functional role of FGF18 in gastric cancer (GC) and elucidate its regulatory mechanisms. The upregulation of FGF18 was detected in seven out of eleven (63.6%) GC cell lines. In primary GC samples, FGF18 was overexpressed in genomically stable and chromosomal instability subtypes of GC and its overexpression was associated with poor survival. Knocking down FGF18 inhibited tumor formation abilities, induced G1 phase cell cycle arrest and enhanced anti-cancer drug sensitivity. Expression microarray profiling revealed that silencing of FGF18 activated ATM pathway but quenched TGF-β pathway. The key factors that altered in the related signaling were validated by western blot and immunofluorescence. Meanwhile, treating GC cells with human recombinant FGF18 or FGF18-conditioned medium accelerated tumor growth through activation of ERK-MAPK signaling. FGF18 was further confirmed to be a direct target of tumor suppressor, miR-590-5p. Their expressions showed a negative correlation in primary GC samples and more importantly, re-overexpression of FGF18 partly abolished the tumor-suppressive effect of miR-590-5p. Our study not only identified that FGF18 serves as a novel prognostic marker and a therapeutic target in GC but also enriched the knowledge of FGF-FGFR signaling during gastric tumorigenesis.
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Registered trials
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