ArticleInternational journal of molecular sciences2021
LEF1 Enhances the Progression of Colonic Adenocarcinoma via Remodeling the Cell Motility Associated Structures.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- LEF1 gene mutation impairs the intestinal barrier and causes diarrhea.Molecular and cellular pediatrics · 2026Article
- Construction of Metastasis Prediction Models and Screening of Anti-Metastatic Drugs Based on Pan-Cancer Single-Cell EMT Features.International journal of molecular sciences · 2025Article
- Machine learning on transcription factor expression profiles for precision breast cancer therapy.Cancer cell international · 2025Article
- Interpretable Multi-Cancer Early Detection Using SHAP-Based Machine Learning on Tumor-Educated Platelet RNA.Diagnostics (Basel, Switzerland) · 2025Article
- Single-Cell RNA Sequencing Reveals LEF1 as a Prognostic Biomarker for Poor Outcomes in Oxaliplatin-Resistant Colorectal Cancer.Human mutation · 2025Article
- Integrating the metabolic and molecular circuits in diabetes, obesity and cancer: a comprehensive review.Discover oncology · 2024Review
- The Interplay among Wnt/β-catenin Family Members in Colorectal Adenomas and Surrounding Tissues.Biomedicines · 2024Article
- Mechanism and role of nuclear laminin B1 in cell senescence and malignant tumors.Cell death discovery · 2024Review
- TCF7L1 regulates colorectal cancer cell migration by repressing GAS1 expression.Scientific reports · 2024Article
- DNA Damage-Induced Apoptosis Suppressor Triggers Progression and Stemness of Glioma by Enhancing Lymphoid Enhancer-Binding Factor 1 Expression.World journal of oncology · 2024Article
- Glucocorticoid receptor: a harmonizer of cellular plasticity in breast cancer-directs the road towards therapy resistance, metastatic progression and recurrence.Cancer metastasis reviews · 2024Review
- Effects of S-Adenosylhomocysteine Hydrolase Downregulation on Wnt Signaling Pathway in SW480 Cells.International journal of molecular sciences · 2023Article
- Epigenome-Wide Changes in the Cell Layers of the Vein Wall When Exposing the Venous Endothelium to Oscillatory Shear Stress.Epigenomes · 2023Article
- The Role of Dendritic Cells in the Host Response to Marek's Disease Virus (MDV) as Shown by Transcriptomic Analysis of Susceptible and Resistant Birds.Pathogens (Basel, Switzerland) · 2022Article
- Molecular Evolution and Inheritance Pattern ofGenes · 2022Article
- Wnt signaling pathway-derived score for predicting therapeutic resistance and tumor microenvironment in lung adenocarcinoma.Frontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lymphoid enhancer-binding factor 1 (LEF1) is a key transcription factor mediating the Wnt signaling pathway. LEF1 is a regulator that is closely associated with tumor malignancy and is usually upregulated in cancers, including colonic adenocarcinoma. The underlying molecular mechanisms of LEF1 regulation for colonic adenocarcinoma progression remain unknown. To explore it, the LEF1 expression in caco2 cells was inhibited using an shRNA approach. The results showed that downregulation of LEF1 inhibited the malignancy and motility associated microstructures, such as polymerization of F-actin, β-tubulin, and Lamin B1 in caco2 cells. LEF1 inhibition suppressed the expression of epithelial/endothelial-mesenchymal transition (EMT) relevant genes. Overall, the current results demonstrated that LEF1 plays a pivotal role in maintaining the malignancy of colonic adenocarcinoma by remodeling motility correlated microstructures and suppressing the expression of EMT-relevant genes. Our study provided evidence of the roles LEF1 played in colonic adenocarcinoma progression, and suggest LEF1 as a potential target for colonic adenocarcinoma therapy.
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