ArticleCell proliferation2019
FOXM1c promotes oesophageal cancer metastasis by transcriptionally regulating IRF1 expression.
Article in Cell proliferation, 2019. 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, 20 citations in OpenAlex.
- IRF1 is a core transcriptional regulatory circuitry member promoting AML progression by regulating lipid metabolism.Experimental hematology & oncology · 2025Article
- The role of kinesin superfamily proteins in hepatocellular carcinoma.Medical oncology (Northwood, London, England) · 2024Review
- The multiple roles of interferon regulatory factor family in health and disease.Signal transduction and targeted therapy · 2024Review
- Roles of Interferon Regulatory Factor 1 in Tumor Progression and Regression: Two Sides of a Coin.International journal of molecular sciences · 2024Review
- Knockdown of UCHL3 inhibits esophageal squamous cell carcinoma progression by reducing CRY2 methylation.Human cell · 2022Article
- The correlation and role analysis of SLC30A1 and SLC30A10 in cervical carcinoma.Journal of Cancer · 2022Article
- A narrative review of research progress on FoxM1 in breast cancer carcinogenesis and therapeutics.Annals of translational medicine · 2021Review
- IRF1 regulates the progression of colorectal cancer via interferon‑induced proteins.International journal of molecular medicine · 2021Article
- Splicing Factor DDX23, Transcriptionally Activated by E2F1, Promotes Ovarian Cancer Progression by Regulating FOXM1.Frontiers in oncology · 2021Article
- FoxM1 is Upregulated in Osteosarcoma and Inhibition of FoxM1 Decreases Osteosarcoma Cell Proliferation, Migration, and Invasion.Cancer management and research · 2020Article
- Maternal Embryonic Leucine Zipper Kinase Promotes Tumor Growth and Metastasis via Stimulating FOXM1 Signaling in Esophageal Squamous Cell Carcinoma.Frontiers in oncology · 2020Article
- FOXM1 promotes hepatocellular carcinoma progression by regulating KIF4A expression.Journal of experimental & clinical cancer research : CR · 2019Article
- FOXM1c promotes oesophageal cancer metastasis by transcriptionally regulating IRF1 expression.Cell proliferation · 2019Article
- IRF1 Negatively Regulates Oncogenic KPNA2 Expression Under Growth Stimulation and Hypoxia in Lung Cancer Cells.OncoTargets and therapy · 2019Article
Corrections and comments
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Authors and funding
20 authors at 3 institutions in 1 country.
Funding
Abstract
objectivesWe aimed to elucidate the role and molecular mechanisms of FOXM1 in regulating metastasis in oesophageal squamous cell carcinoma (ESCC) as well as its clinical implications. MATERIALS AND
methodsThe expression levels of four isoforms of FOXM1 were analysed by real-time PCR. Next, genetically modification using overexpression and RNAi systems and transwell were employed to examine FOXM1c function in invasion and migration. Dual luciferase and ChIP assays were performed to decipher the underlying mechanism for transcriptional regulation. The expression levels of FOXM1 and IRF1 were determined by immunohistochemistry staining in ESCC specimens.
resultsThe FOXM1c was predominantly overexpressed in ESCC cell lines compared to the other FOXM1 isoforms. Ectopic expression of FOXM1c promoted invasion and migration of ESCC cells lines, whereas downregulation of FOXM1c inhibited these processes. Moreover, FOXM1c expression was positively correlated with IRF1 expression in ESCC cell lines and tumour specimens. IRF1 is, at least in part, responsible for FOXM1c-mediated invasion and migration. Mechanistically, we identified IRF1 as a transcriptional target of FOXM1c and found a FOXM1c-binding site in the IRF1 promoter region. Furthermore, high expression levels of both FOXM1c and IRF1 were positively associated with low survival rate and predicted a poor prognosis of oesophageal cancer patients.
conclusionFOXM1c promotes the metastasis by transcriptionally targeting IRF1 and may serve as a potential prognostic predictor for oesophageal cancer.
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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.