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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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Krüppel-like Factor 13 Promotes HCC Progression by Transcriptional Regulation of HMGCS1-mediated Cholesterol Synthesis

TL;DR: In this article , the role and potential molecular mechanism of KLF13 in the growth and migration of liver cancer cells was explored, where the authors used real-time quantitative polymerase chain reaction (qPCR) and western blotting to detect mRNA and protein expression in HCC tissues and cells.
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Characterization and Spatiotemporal Expression of Klf4 in Large Yellow Croaker Larimichthys crocea.

TL;DR: The spatiotemporal expression patterns of Lc-Klf4 illustrated that Klf4 involves in spermatogenesis, embryogenesis, and adult physiological processes.
Journal Article

The aberrant expressions of MACC1, ZEB1, and KLF4 in hepatocellular carcinoma and their clinical significance.

TL;DR: Positive expressions of MACC1, ZEB1, and KLF4 should be correlated with the duration of OS in patients with HCC and considered promising prognostic biomarkers, as well as potential therapeutic targets for HCC.
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Silencing KLF16 inhibits oral squamous cell carcinoma cell proliferation by arresting the cell cycle and inducing apoptosis.

TL;DR: In this paper, the role of KLF16 in oral squamous cell carcinoma (OSCC) remains unknown, and the authors conducted a study to investigate its related mechanism.
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KLF16 inhibits PEDV replication by activating the type I IFN signaling pathway.

TL;DR: In this paper , the role of KLF16 in viral replication and the signaling mechanism of type I IFN was investigated and it was found that over-expression of KLf16 inhibited the replication of porcine epidemic diarrhea virus (PEDV) through the type I ILP signaling pathway.
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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