ArticleThe Kaohsiung journal of medical sciences2023
ZNF521/EBF1 axis regulates AKR1B1 to promote the proliferation, migration, and invasion of gastric cancer cells.
Article in The Kaohsiung journal of medical sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 12 citations in OpenAlex.
- Transcription Activation of DEPDC1B Upon EBF1 Loss Contributes to Cell Cycle Progression and Epithelial-Mesenchymal Transition in Colon Adenocarcinoma.Biochemical genetics · 2026Article
- Luteolin inhibits hyperglycemia-induced epithelial-mesenchymal transition and malignant progression in gastric cancer via targeting AKR1B1-mediated glucose metabolism.Clinical & experimental metastasis · 2026Article
- A prediction model of gastric cancer based on M2-like tumor-associated macrophage infiltration verified by immunohistochemistry.Translational cancer research · 2026Article
- EBF1 Deficiency Drives Prostate Cancer Progression by Interfering with the Transcriptional Regulation ofOncology research · 2026Article
- Bulk and single-cell transcriptomics of stomach adenocarcinoma provide prognostic insights via the application of a novel gene signature associated with manganese metabolism.Translational cancer research · 2025Article
- Advances in Research on the B-Lineage Transcription Factor EBF1 in Solid Tumors.International journal of molecular sciences · 2025Review
- Efficient and accurate framework for genome-wide gene-environment interaction analysis in large-scale biobanks.Nature communications · 2025Article
- ZNF521 promotes acute myeloid leukemogenesis by suppressing the expression and acetylation of SMC3.Heliyon · 2024Article
- Exploring the metastasis-related biomarker and carcinogenic mechanism in liver cancer based on single cell technology.Heliyon · 2024Article
- Lipid Metabolism-Related Gene Signature Predicts Prognosis and Indicates Immune Microenvironment Infiltration in Advanced Gastric Cancer.Gastroenterology research and practice · 2024Article
- Aldo-keto reductases: Role in cancer development and theranostics.Oncology research · 2024Review
- Focusing on the Immune Cells: Recent Advances in Immunotherapy for Biliary Tract Cancer.Cancer management and research · 2024Review
- Research of restricted migration evaluation of MDA-MB-231 cells in 2D and 3D co-culture models.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Zinc Finger 521 Modulates the Nrf2-Notch Signaling Pathway in Human Ovarian Carcinoma.International journal of molecular sciences · 2023Article
- ZNF521/EBF1 axis regulates AKR1B1 to promote the proliferation, migration, and invasion of gastric cancer cells.The Kaohsiung journal of medical sciences · 2023Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the incidence and death rates of gastric cancer (GC) are decreasing, approximately one million new cases and 800,000 GC-related deaths were reported worldwide in 2018. Currently, the oncogenesis of GC remains unclear, and the demand for novel treatment options are unmet. Here, we explored the role of aldo-keto reductase family 1 member B (AKR1B1) in the progression of GC. The proliferation, migration, and invasion of GC cells were evaluated by CCK-8 assay, wound healing assay, and transwell assay, respectively. The interaction between EBF transcription factor 1 (EBF1) and the promoter region of AKR1B1 was determined by luciferase reporter assay and chromatin immunoprecipitation (ChIP). Gene expression levels were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting assay. The expression of AKR1B1 was elevated in GC cells, resulting in increased cell proliferation, migration, and invasion. Meanwhile, EBF1 was a negative regulator of AKR1B1; its overexpression suppressed AKR1B1 expression and GC progression. Furthermore, knockdown of ZNF521 induced EBF1 expression, thus suppressing AKR1B1 expression and resulting in attenuated GC growth and invasiveness. Notably, knockdown of ZNF521 attenuated GC progression and was rescued by overexpression of AKR1B1. Our current study revealed a novel ZNF521/EBF1/AKR1B1 axis in GC and elaborated its important role in promoting GC progression, providing potential therapeutic targets for anti-GC treatments.
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