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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 transcription factor Klf5 is essential for intrahepatic biliary epithelial tissue remodeling after cholestatic liver injury

TL;DR: It is demonstrated that the transcription factor Krüppel-like factor 5 (Klf5) is highly enriched in mouse liver BECs and plays a key role in regulating the ductular reaction, specifically under cholestatic injury conditions.
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KLF16 Affects the MYC Signature and Tumor Growth in Prostate Cancer.

TL;DR: In vitro and in vivo experiments both demonstrated that depleting KLF16 significantly inhibited the growth of PCa cells, and bioinformatics analysis showed that KLf16 may be required for PCa development.
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Radiotherapy in combination with hyperthermia suppresses lung cancer progression via increased NR4A3 and KLF11 expression

TL;DR: The results suggest that NR4A3 and KLF11 are critical for increasing the efficacy of radiotherapy in combination with HT, and the effect of these two factors on lung cancer progression was evaluated by in vivo xenograft studies.
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Whole exome sequencing of multiple meningiomas with varying histopathological presentation in one patient revealed distinctive somatic mutation burden and independent clonal origins.

TL;DR: The data suggest the two meningiomas might develop independently in this patient and molecular subtyping by NGS is a valuable supplement to conventional pathology.
References
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Macrophage plasticity and interaction with lymphocyte subsets: cancer as a paradigm

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