Abstract
Gastrointestinal (GI) cancer is characterized by its aggressiveness, but the underlying mechanism is not fully understood. Studies reveal that epithelial to mesenchymal transition (EMT), which is regulated by a series of transcription factors and signaling pathways, is strongly associated with GI cancer cell proliferation, invasion and metastasis. Importantly, EMT is a product of crosstalk between signaling pathways. Krüppel-like factor 4 (KLF4), a zinc finger-type transcription factor, is decreased or lost in most GI cancers. By transcriptionally regulating its downstream target genes, KLF4 plays important roles of GI cancer tumorigenesis, proliferation and differentiation. In this review, we focus on the mechanism of KLF4 in GI cancer EMT, and demonstrate that through crosstalk with TGF-β, Notch, and Wnt signaling pathways, KLF4 negatively regulates EMT of GI cancers. Finally, we indicate the challenging new frontiers for KLF4 which contributes to better understanding of the mechanism of GI cancer aggressiveness.
Keywords: EMT, gastrointestinal cancer, KLF4, Notch, TGF-β, Wnt.
Current Cancer Drug Targets
Title:Regulation of EMT by KLF4 in Gastrointestinal Cancer
Volume: 13 Issue: 9
Author(s): Jiujie Cui, Min Shi, Ming Quan and Keping Xie
Affiliation:
Keywords: EMT, gastrointestinal cancer, KLF4, Notch, TGF-β, Wnt.
Abstract: Gastrointestinal (GI) cancer is characterized by its aggressiveness, but the underlying mechanism is not fully understood. Studies reveal that epithelial to mesenchymal transition (EMT), which is regulated by a series of transcription factors and signaling pathways, is strongly associated with GI cancer cell proliferation, invasion and metastasis. Importantly, EMT is a product of crosstalk between signaling pathways. Krüppel-like factor 4 (KLF4), a zinc finger-type transcription factor, is decreased or lost in most GI cancers. By transcriptionally regulating its downstream target genes, KLF4 plays important roles of GI cancer tumorigenesis, proliferation and differentiation. In this review, we focus on the mechanism of KLF4 in GI cancer EMT, and demonstrate that through crosstalk with TGF-β, Notch, and Wnt signaling pathways, KLF4 negatively regulates EMT of GI cancers. Finally, we indicate the challenging new frontiers for KLF4 which contributes to better understanding of the mechanism of GI cancer aggressiveness.
Export Options
About this article
Cite this article as:
Cui Jiujie, Shi Min, Quan Ming and Xie Keping, Regulation of EMT by KLF4 in Gastrointestinal Cancer, Current Cancer Drug Targets 2013; 13 (9) . https://dx.doi.org/10.2174/15680096113136660104
DOI https://dx.doi.org/10.2174/15680096113136660104 |
Print ISSN 1568-0096 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5576 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
NK-1 Receptor Antagonists: A New Paradigm in Pharmacological Therapy
Current Medicinal Chemistry Fluorescence Imaging in Cancerology
Current Molecular Imaging (Discontinued) Marine Collagen as a Source of Bioactive Molecules: A Review
The Natural Products Journal Plant Troponoids: Chemistry, Biological Activity, and Biosynthesis
Current Medicinal Chemistry Novel VEGF-independent Strategies Targeting Tumor Vasculature: Clinical Aspects
Current Pharmaceutical Design Breast Cancer: Understanding Sensitivity and Resistance to Chemotherapy and Targeted Therapies to Aid in Personalised Medicine
Current Cancer Drug Targets Bioavailability and Pharmacokinetics of Genistein: Mechanistic Studies on its ADME
Anti-Cancer Agents in Medicinal Chemistry Molecular Targets of Omega-3 Fatty Acids for Cancer Therapy
Anti-Cancer Agents in Medicinal Chemistry Quassinoids: From Traditional Drugs to New Cancer Therapeutics
Current Medicinal Chemistry Therapeutic Dilemma in Personalized Medicine
Current Reviews in Clinical and Experimental Pharmacology Anti-inflammatory Effects of Dietary Antioxidants
Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents Meet Our Regional Editor
Current Gene Therapy Neglected Tropical Protozoan Diseases: Drug Repositioning as a Rational Option
Current Topics in Medicinal Chemistry STAT3: A Molecular Target for Cancer Whose Time Has Come
Current Signal Transduction Therapy 1,5-Dioxaspiro[2.4]heptanes
Current Chemical Biology Pd-Catalyzed N-arylation of 2-imidazolines Provides Convenient Access to Selective Cyclooxygenase-2 Inhibitors
Letters in Organic Chemistry CEACAM1 in Malignant Melanoma: A Diagnostic and Therapeutic Target
Current Topics in Medicinal Chemistry Tailored Angiogenesis Inhibition in Cancer Therapy: Respecting the Heart to Improve the Net Outcome
Current Signal Transduction Therapy Nanocrystals: From Raw Material to the Final Formulated Oral Dosage Form - A Review
Current Pharmaceutical Design Radiolabeled Sugars Used for PET and SPECT Imaging
Current Radiopharmaceuticals