ArticleCancers2021
KLF4 Induces Mesenchymal-Epithelial Transition (MET) by Suppressing Multiple EMT-Inducing Transcription Factors.
Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 37 citations in OpenAlex.
- Adaptive epithelial-mesenchymal bi-directional transition: A key invasive plasticity for tumor metastasis.iScience · 2026Review
- Fluctuating environment causes neoplastic transition and epithelial-mesenchymal plasticity in human cells.Research square · 2026Article
- Epithelial-Mesenchymal Plasticity in Cancer: Transcriptional Regulation, Biomarker Challenges, and Emerging Therapeutic Opportunities.Cell biochemistry and function · 2026Review
- Systems-level analysis identifies IRF6 as an inhibitor of epithelial-mesenchymal transition.Journal of biological engineering · 2026Article
- Multi-Protein Profiling Reveals High Nuclear KFL-4 Expression as a Predictor of Poor Overall Survival in Breast Cancer: A Retrospective Cohort Study.International journal of molecular sciences · 2026Article
- Epithelial-mesenchymal transition and sunitinib resistance in renal cell carcinoma: mechanisms and therapeutic strategies.Frontiers in pharmacology · 2026Review
- Postbiotics Combination Synergises the Antiproliferative Effects of Doxorubicin in Gastric Cancer Cells: A Cellular and Molecular Deep Dive.International journal of molecular sciences · 2025Article
- CAF derived IL-33 mediated EMT to promote the metastasis of LSCC cells.European journal of medical research · 2025Article
- HOXA10-TWIST2 antagonism drives partial epithelial-to-mesenchymal transition for embryo implantation.Cell death discovery · 2025Article
- Review
- Endocardial primary cilia and blood flow regulate EndoMT during endocardial cushion development.Nature cardiovascular research · 2025Article
- Article
- Aurora kinase A promotes epithelial‑mesenchymal transition by regulating P130 and P107 molecules in thyroid cancer cells.Experimental and therapeutic medicine · 2025Article
- Harnessing the tumor microenvironment: targeted cancer therapies through modulation of epithelial-mesenchymal transition.Journal of hematology & oncology · 2025Review
- Mechanism of KLF4 Inhibition of epithelial-mesenchymal transition in gastric cancer cells.Open life sciences · 2025Article
- ZEB2 drives intra-tumor heterogeneity and skin squamous cell carcinoma formation with distinct EMP transition states.iScience · 2024Article
- KLF4 Induces Colorectal Cancer by Promoting EMT via STAT3 Activation.Digestive diseases and sciences · 2024Article
- Article
- Leveraging Cancer Phenotypic Plasticity for Novel Treatment Strategies.Journal of clinical medicine · 2024Article
- Transcriptional state dynamics lead to heterogeneity and adaptive tumor evolution in urothelial bladder carcinoma.Communications biology · 2023Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Epithelial-Mesenchymal Plasticity (EMP) refers to reversible dynamic processes where cells can transition from epithelial to mesenchymal (EMT) or from mesenchymal to epithelial (MET) phenotypes. Both these processes are modulated by multiple transcription factors acting in concert. While EMT-inducing transcription factors (TFs)-TWIST1/2, ZEB1/2, SNAIL1/2/3, GSC, and FOXC2-are well-characterized, the MET-inducing TFs are relatively poorly understood (OVOL1/2 and GRHL1/2). Here, using mechanism-based mathematical modeling, we show that transcription factor KLF4 can delay the onset of EMT by suppressing multiple EMT-TFs. Our simulations suggest that KLF4 overexpression can promote a phenotypic shift toward a more epithelial state, an observation suggested by the negative correlation of KLF4 with EMT-TFs and with transcriptomic-based EMT scoring metrics in cancer cell lines. We also show that the influence of KLF4 in modulating the EMT dynamics can be strengthened by its ability to inhibit cell-state transitions at the epigenetic level. Thus, KLF4 can inhibit EMT through multiple parallel paths and can act as a putative MET-TF. KLF4 associates with the patient survival metrics across multiple cancers in a context-specific manner, highlighting the complex association of EMP with patient survival.
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Registered trials
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 Socratic graph.