ArticleThe Journal of biological chemistry2014
FGF16 promotes invasive behavior of SKOV-3 ovarian cancer cells through activation of mitogen-activated protein kinase (MAPK) signaling pathway.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 44 citations in OpenAlex.
- RAS/Mitogen-Activated Protein Kinase Signaling Pathway in Testicular Germ Cell Tumors.Life (Basel, Switzerland) · 2024Review
- Identification and Comparative Analysis of Long Non-coding RNAs in High- and Low-Fecundity Goat Ovaries During Estrus.Frontiers in genetics · 2021Article
- FGF16 regulated by miR-520b enhances the cell proliferation of lung cancer.Open medicine (Warsaw, Poland) · 2021Article
- FGF/FGFR signaling in health and disease.Signal transduction and targeted therapy · 2020Review
- Article
- TRIM21 causes abnormal expression of IL-6 in oral lichen planus via the TRIB2-MAPK signal axis.American journal of translational research · 2020Article
- MiRNA-144-3p inhibits high glucose induced cell proliferation through suppressing FGF16.Bioscience reports · 2019Article
- Breakpoint mapping at nucleotide resolution in X-autosome balanced translocations associated with clinical phenotypes.European journal of human genetics : EJHG · 2019Article
- Increased Expression of Holliday Junction-Recognizing Protein (HJURP) as an Independent Prognostic Biomarker in Advanced-Stage Serous Ovarian Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Salvianolic acid B suppresses cell proliferation and induces apoptosis in osteosarcoma through p38-mediated reactive oxygen species generation.Oncology letters · 2018Article
- MiR-520f promotes cell aggressiveness by regulating fibroblast growth factor 16 in hepatocellular carcinoma.Oncotarget · 2017Article
- Gene regulatory networking reveals the molecular cue to lysophosphatidic acid-induced metabolic adaptations in ovarian cancer cells.Molecular oncology · 2017Article
- FGFs: crucial factors that regulate tumour initiation and progression.Cell proliferation · 2016Review
- Regulatory Differences in Natal Down Development between Altricial Zebra Finch and Precocial Chicken.Molecular biology and evolution · 2016Article
- Characterization of FGFR signaling pathway as therapeutic targets for sarcoma patients.Cancer biology & medicine · 2016Article
- Smad4-dependent suppressor pituitary homeobox 2 promotes PPP2R2A-mediated inhibition of Akt pathway in pancreatic cancer.Oncotarget · 2016Article
- Ubiquitin-specific protease 7 expression is a prognostic factor in epithelial ovarian cancer and correlates with lymph node metastasis.OncoTargets and therapy · 2016Article
- Invasion of ovarian cancer cells is induced byPITX2-mediated activation of TGF-β and Activin-A.Molecular cancer · 2015Article
- FGF signaling supports Drosophila fertility by regulating development of ovarian muscle tissues.Developmental biology · 2015Article
- Hepatoma-derived growth factor predicts unfavorable prognosis of epithelial ovarian cancer.OncoTargets and therapy · 2015Article
Corrections and comments
- Retraction · 2020-12-11Duplication of/in Image · Manipulation of Images ·
- Retracted
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Uncontrolled cell growth and tissue invasion define the characteristic features of cancer. Several growth factors regulate these processes by inducing specific signaling pathways. We show that FGF16, a novel factor, is expressed in human ovary, and its expression is markedly increased in ovarian tumors. This finding indicated possible involvement of FGF16 in ovarian cancer progression. We observed that FGF16 stimulates the proliferation of human ovarian adenocarcinoma cells, SKOV-3 and OAW-42. Furthermore, through the activation of FGF receptor-mediated intracellular MAPK pathway, FGF16 regulates the expression of MMP2, MMP9, SNAI1, and CDH1 and thus facilitates cellular invasion. Inhibition of FGFR as well as MAPK pathway reduces the proliferative and invasive behavior of ovarian cancer cells. Moreover, ovarian tumors with up-regulated PITX2 expression also showed activation of Wnt/β-catenin pathway that prompted us to investigate possible interaction among FGF16, PITX2, and Wnt pathway. We identified that PITX2 homeodomain transcription factor interacts with and regulates FGF16 expression. Furthermore, activation of the Wnt/β-catenin pathway induces FGF16 expression. Moreover, FGF16 promoter possesses the binding elements of PITX2 as well as T-cell factor (Wnt-responsive), in close proximity, where PITX2 and β-catenin binds to and synergistically activates the same. A detail study showed that both PITX2 and T-cell factor elements and the interaction with their binding partners are necessary for target gene expression. Taken together, our findings indicate that FGF16 in conjunction with Wnt pathway contributes to the cancer phenotype of ovarian cells and suggests that modulation of its expression in ovarian cells might be a promising therapeutic strategy for the treatment of invasive ovarian cancers.
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