ArticleThe American journal of pathology2010
Reduced expression of fibroblast growth factor receptor 2IIIb in hepatocellular carcinoma induces a more aggressive growth.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 58 citations in OpenAlex.
- Identification of DYNLL1 and FGFR2 as potential apoptosis-associated biomarkers in HBV-related hepatocellular carcinoma.Discover oncology · 2026Article
- Characterization of Alternative Splicing in High-Risk Wilms' Tumors.International journal of molecular sciences · 2024Article
- The Long Non-Coding RNA ANRIL in Cancers.Cancers · 2023Review
- The interplay between non-coding RNAs and alternative splicing: from regulatory mechanism to therapeutic implications in cancer.Theranostics · 2023Review
- Inferring cancer common and specific gene networks via multi-layer joint graphical model.Computational and structural biotechnology journal · 2023Article
- Spatial expression of the FGFR2b splice isoform and its prognostic significance in endometrioid endometrial carcinoma.The journal of pathology. Clinical research · 2022Article
- Integrated DNA Copy Number and Expression Profiling Identifies IGF1R as a Prognostic Biomarker in Pediatric Osteosarcoma.International journal of molecular sciences · 2022Article
- Long non-coding RNAs are involved in alternative splicing and promote cancer progression.British journal of cancer · 2022Review
- Review
- Fibroblast Growth Factor Receptors (FGFRs) and Noncanonical Partners in Cancer Signaling.Cells · 2021Review
- Article
- Noncoding RNAs regulate alternative splicing in Cancer.Journal of experimental & clinical cancer research : CR · 2021Review
- 2b or Not 2b: How Opposing FGF Receptor Splice Variants Are Blocking Progress in Precision Oncology.Journal of oncology · 2021Review
- Alternative splicing modulates cancer aggressiveness: role in EMT/metastasis and chemoresistance.Molecular biology reports · 2021Review
- Advances of Fibroblast Growth Factor/Receptor Signaling Pathway in Hepatocellular Carcinoma and its Pharmacotherapeutic Targets.Frontiers in pharmacology · 2021Review
- Hormonal Receptor Status Determines Prognostic Significance of FGFR2 in Invasive Breast Carcinoma.Cancers · 2020Article
- Molecular crosstalk between Y5 receptor and neuropeptide Y drives liver cancer.The Journal of clinical investigation · 2020Article
- Fibroblast growth factor 7 signalling is disrupted in colorectal cancer and is a potential marker of field cancerisation.Journal of gastrointestinal oncology · 2019Article
- DEIsoM: a hierarchical Bayesian model for identifying differentially expressed isoforms using biological replicates.Bioinformatics (Oxford, England) · 2017Article
- miR-494 inhibits ovarian cancer cell proliferation and promotes apoptosis by targeting FGFR2.Oncology letters · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibroblast growth factor receptor 2 isoform b (FGFR2-IIIb) is highly expressed in hepatocytes and plays an important role in liver homeostasis and regeneration. Here, we analyzed the expression and function of FGFR2-IIIb in hepatocellular carcinoma (HCC). FGFR2-IIIb expression in HCC tissues and cell lines was lower than in primary human hepatocytes and nontumorous tissue. FGFR2-IIIb-negative HCCs showed a significantly higher Ki-67 labeling index, and loss of FGFR2-IIIb expression correlated significantly with vascular invasion and more advanced tumor stages. A decrease in FGFR-2IIIb expression in HCC cell lines was not related to promoter hypermethylation. However, PCR analysis indicated that chromosomal deletion at 10q accounted for the loss of FGFR2 expression in a subset of HCC cells. FGFR2-IIIb re-expression in stable transfected HCC cell lines induced a higher basal apoptosis rate and a significantly reduced proliferation and migratory potential in vitro. In nude mice, FGFR2-IIIb re-expressing HCC cells grew significantly slower, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay revealed higher apoptosis rates. The antitumorigenic effects of FGFR2-IIIb expression in HCC cells were not affected by keratinocyte growth factor or an inhibitor of FGFR-phosphorylation, indicating that they are independent of tyrosine kinase activation. In conclusion, our data indicate that FGFR2-IIIb inhibits tumorigenicity of HCC cells. Identification of the molecular mechanisms promoting regeneration in normal tissue while suppressing malignancy may lead to novel therapeutic targets of this highly aggressive tumor.
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