ArticleOncology reports2017
c-Fos mediates α1, 2-fucosyltransferase 1 and Lewis y expression in response to TGF-β1 in ovarian cancer.
Article in Oncology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- microRNAs bidirectionally regulate FUT1 to modulate α-1,2-fucosylation and cancer-associated biology.The Journal of biological chemistry · 2026Article
- FUT3 mediated GRP78 fucosylation promotes colorectal cancer survival and proliferation under glucose restriction via PERK/ATF4/STC2 axis.NPJ precision oncology · 2025Article
- Article
- C-FOS inhibition promotes pancreatic cancer cell ferroptosis by transcriptionally regulating the expression of SLC7A11.Functional & integrative genomics · 2024Article
- Article
- FUT1-mediated terminal fucosylation acts as a new target to attenuate renal fibrosis.Molecular medicine (Cambridge, Mass.) · 2023Article
- Role of different non-coding RNAs as ovarian cancer biomarkers.Journal of ovarian research · 2022Review
- Human Epididymis Protein 4 and Lewis y Enhance Chemotherapeutic Resistance in Epithelial Ovarian Cancer Through the p38 MAPK Pathway.Advances in therapy · 2022Article
- Carcinoembryonic antigen as a specific glycoprotein ligand of rBC2LCN lectin on pancreatic ductal adenocarcinoma cells.Cancer science · 2021Article
- Laminin γ2-mediating T cell exclusion attenuates response to anti-PD-1 therapy.Science advances · 2021Article
- UBE2N Regulates Paclitaxel Sensitivity of Ovarian Cancer via Fos/P53 Axis.OncoTargets and therapy · 2020Article
- Expression and function of FRA1 protein in tumors.Molecular biology reports · 2020Review
- The Jun N-terminal kinases signaling pathway plays a "seesaw" role in ovarian carcinoma: a molecular aspect.Journal of ovarian research · 2019Review
- The Diverse Contributions of Fucose Linkages in Cancer.Cancers · 2019Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FUT1 is a key rate-limiting enzyme in the synthesis of Lewis y, a membrane-associated carbohydrate antigen. The aberrant upregulation of FUT1 and Lewis y antigen is related to proliferation, invasion and prognosis in malignant epithelial tumors. A c-Fos/activator protein-1 (AP-1) binding site was found in the FUT1 promoter. However, the mechanisms of transcriptional regulation of FUT1 remain poorly understood. TGF-β1 is positively correlated to Lewis y. In the present study, we investigated the molecular mechanism of FUT1 gene expression in response to TGF-β1. We demonstrated that c-Fos was highly expressed in 77.50% of ovarian epithelial carcinoma cases and was significantly correlated with Lewis y. Using luciferase activity and chromatin immunoprecipitation (ChIP) assay, we further revealed that c-Fos interacted with the FUT1 promoter in ovarian cancer cells and transcriptional capacity of the heterodimer formed by c-Fos and c-Jun was stronger than that of the c-Fos or c-Jun homodimers. Then, we demonstrated that TGF-β1 induced dose-dependent c-Fos expression, which was involved in TGF-β1-induced ovarian cancer cell proliferation. In addition, inhibition of MAPK activation or TGF-β1 receptor by pharmacological agents prevented TGF-β1-induced c-Fos and Lewis y expression. Silencing of c-Fos prevented TGF-β1-induced Lewis y expression. Collectively, the results of these studies demonstrated that TGF-β1 regulated FUT1 and Lewis y expression by activating the MAPK/c-Fos pathway.
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