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Krüppel-like factors in cancer

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TLDR
The roles and regulation of the 17 known KLFs in various cancer-relevant processes are discussed, with some KLFs having different roles in normal cells and cancer, during cancer development and progression and in different cancer types.
Abstract
Kruppel-like factors (KLFs) are a family of DNA-binding transcriptional regulators with diverse and essential functions in a multitude of cellular processes, including proliferation, differentiation, migration, inflammation and pluripotency. In this Review, we discuss the roles and regulation of the 17 known KLFs in various cancer-relevant processes. Importantly, the functions of KLFs are context dependent, with some KLFs having different roles in normal cells and cancer, during cancer development and progression and in different cancer types. We also identify key questions for the field that are likely to lead to important new translational research and discoveries in cancer biology.

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The roles of zinc finger proteins in non-alcoholic fatty liver disease

TL;DR: The current knowledge of several ZFPs that play critical roles in the progression of non-alcoholic fatty liver disease are highlighted, their mechanistic functional networks are described, and the potential for Z FPs as therapeutic targets for NAFLD is discussed.

Protective Effects of Krüppel- Like Factor 4 against Cardiovascular Disease

TL;DR: The functions of KLF4 in cardiovascular diseases are reviewed to show that deletion of the Klf4 gene accelerates neointimal formation following vascular injury and results in enhanced atherosclerotic lesion formation.
Journal ArticleDOI

KLF11 promotes the progression of glioma via regulating HJURP.

TL;DR: It is found that KLF11 was highly expressed in glioma cancer tissues and cells, and KLF 11 high expression of glioblastoma and Lower-grade gliomas were correlated with poorer overall survival and disease-free survival percentages.
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Arginine methylation in the epithelial-to-mesenchymal transition.

TL;DR: In this article, a review of arginine methylation-dependent mechanisms that regulate EMT in the aspects of signaling, transcriptional, and splicing regulation is presented. But, the authors do not consider the role of the post-transcriptional, translational, and posttranslational mechanisms.
Journal ArticleDOI

KLF11 promotes the progression of glioma via regulating Holliday junction recognition protein

TL;DR: The function of KLF11 in glioma is demonstrated and it is shown KLF 11 and HJURP could be prognostic and diagnostic markers inglioma, which provides a new insight of gliomas therapy.
References
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Epithelial-Mesenchymal Transitions in Development and Disease

TL;DR: The mesenchymal state is associated with the capacity of cells to migrate to distant organs and maintain stemness, allowing their subsequent differentiation into multiple cell types during development and the initiation of metastasis.
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Wnt/beta-catenin signaling in development and disease.

TL;DR: A remarkable interdisciplinary effort has unraveled the WNT (Wingless and INT-1) signal transduction cascade over the last two decades, finding that Germline mutations in the Wnt pathway cause several hereditary diseases, and somatic mutations are associated with cancer of the intestine and a variety of other tissues.
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Lessons from Hereditary Colorectal Cancer

TL;DR: The authors are grateful to the members of their laboratories for their contributions to the reviewed studies and to F. Giardiello and S. Hamilton for photographs of colorectal lesions.
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Phylogeny.fr: robust phylogenetic analysis for the non-specialist

TL;DR: The Phylogeny.fr platform transparently chains programs to automatically perform phylogenetic analyses and can also meet the needs of specialists; the first ones will find up-to-date tools chained in a phylogeny pipeline to analyze their data in a simple and robust way, while the specialists will be able to easily build and run sophisticated analyses.
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Macrophage plasticity and interaction with lymphocyte subsets: cancer as a paradigm

TL;DR: A better understanding of the molecular basis of myelomonocytic cell plasticity will open new vistas in immunopathology and therapeutic intervention and provide a paradigm for macrophage plasticity and function.
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