ArticleCell death & disease2016
Direct regulation of FOXK1 by C-jun promotes proliferation, invasion and metastasis in gastric cancer cells.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 89 citations in OpenAlex.
- FOXK1: a multifaceted regulator in metabolic reprogramming and disease progression.Biology direct · 2026Review
- RNA‑binding protein DAZAP1 promotes gastric cancer metastasis by enhancing NOTCH1 and JAG1 mRNA stability.International journal of oncology · 2026Article
- Adipose tissue-derived stromal cells enhance glycolytic metabolism in injured nerve cells via the FOXK1-HK2 axis for spinal cord injury repair.Journal of translational medicine · 2026Article
- SWI/SNF ATPase silenced HLF potentiates lung metastasis in solid cancers.Nature communications · 2025Article
- The LncRNA lnc-POTEM-4:14 promotes HCC progression by interacting with FOXK1.Scientific reports · 2025Article
- Protein phosphatase 1 regulatory subunit 15 A (PPP1R15A) promoted the progression of gastric cancer by activating cell autophagy under energy stress.Journal of experimental & clinical cancer research : CR · 2025Article
- Circular RNA Circ_0079226 Plays an Oncogenic Role in Gastric Cancer via the miR-155-5p/FOXK1/AKT Pathway.Analytical cellular pathology (Amsterdam) · 2025Article
- Identification of GPX3 and JUN as Tumor Suppressors in Thyroid Cancer through Integrated WGCNA and Mendelian Randomization.Journal of Cancer · 2025Article
- Single-cell multi-omics sequencing uncovers region-specific plasticity of glioblastoma for complementary therapeutic targeting.Science advances · 2024Article
- Forkhead Box Protein K1 Promotes Chronic Kidney Disease by Driving Glycolysis in Tubular Epithelial Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Biochemical and cellular insights into the Baz2B protein, a non-catalytic subunit of the chromatin remodeling complex.Nucleic acids research · 2024Article
- Exploring the mechanism of ellagic acid against gastric cancer based on bioinformatics analysis and network pharmacology.Journal of cellular and molecular medicine · 2023Article
- FOXK1 regulates epithelial-mesenchymal transition and radiation sensitivity in nasopharyngeal carcinoma via the JAK/STAT3 signaling pathway.Genes & genomics · 2023Article
- miR-144-3p represses hepatocellular carcinoma progression by affecting cell aerobic glycolysis via FOXK1.International journal of experimental pathology · 2023Article
- FOXK1 regulates malignant progression and radiosensitivity through direct transcriptional activation of CDC25A and CDK4 in esophageal squamous cell carcinoma.Scientific reports · 2023Article
- The Role of Polo-Like Kinase 1 in Regulating the Forkhead Box Family Transcription Factors.Cells · 2023Review
- JLP/Foxk1/N-cadherin axis fosters a partial epithelial-mesenchymal transition state in epithelial tubular cells.iScience · 2023Article
- Transcription factor c-Jun modulates GLUT1 in glycolysis and breast cancer metastasis.BMC cancer · 2022Article
- FOXK2 promotes ovarian cancer stemness by regulating the unfolded protein response pathway.The Journal of clinical investigation · 2022Article
- The Function of FoxK Transcription Factors in Diseases.Frontiers in physiology · 2022Review
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Forkhead box (FOX) K1 is a member of the FOX transcription factor superfamily. High FOXK1 expression is associated with several cancers. However, whether FOXK1 expression contributes to gastric cancer (GC) development and progression remains unknown. We analyzed the FOXK1 promoter using the Promo software and found several binding sequence transcription factors, including c-jun. However, the molecular mechanism by which FOXK1 affects the c-jun-mediated malignant phenotype is poorly understood. Here, we found that FOXK1 protein expression was higher in 8/10 (80.0%) fresh cancer tissues compared with that in adjacent normal tissues. FOXK1 overexpression enhanced the proliferation, migration and invasion of GC cells. Moreover, FOXK1 expression was stimulated by transforming growth factor-β1 (TGF-β1). FOXK1 acted as a potential epithelial-to-mesenchymal transition (EMT) inducer by stimulating vimentin expression and inducing the loss of E-cadherin in stable FOXK1-transfected cells. The results of promoter reporter and chromatin immunoprecipitation assays demonstrated that c-jun directly binds to and activates the human FOXK1 gene promoter. A positive correlation was observed between the expression patterns of FOXK1 and c-jun in GC cells and tissue. FOXK1 and c-jun expression were correlated with tumor progression and represented significant predictors of overall survival in GC patients. However, the siRNA-mediated repression of c-jun in FOXK1-overexpressing cells reversed EMT, as well as the proliferative and metastatic phenotypes. In vivo, c-jun promoted FOXK1-mediated proliferation and metastasis via orthotopic implantation. The evidence presented here suggests that FOXK1-directed regulation by c-jun promote the development and progression of human GC.
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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.