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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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Role of Krüppel-Like Factor 4 in the Maintenance of Chemoresistance of Anaplastic Thyroid Cancer

TL;DR: KLF4 is identified as a potential therapeutic target for eliminating ATC cells, and KLF4 expression is necessary for maintaining the undifferentiated phenotype and drug resistance in vitro and in vivo.
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Role of microRNAs in regulating cell proliferation, metastasis and chemoresistance and their applications as cancer biomarkers in small cell lung cancer.

TL;DR: In this paper, the role of microRNAs (miRNAs) in regulating the biological process in small cell lung cancer (SCLC) was comprehensively discussed and evaluated.
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CNOT3 targets negative cell cycle regulators in non-small cell lung cancer development.

TL;DR: It is proposed that the up-regulation of CNOT3 facilitates the development of non-small cell lung cancer through down- regulation of Krüppel-like factor 2 and p21, contrary to tumor suppressive functions of C NOT3 in T-ALL.
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Novel crosstalk between KLF4 and ZEB1 regulates gemcitabine resistance in pancreatic ductal adenocarcinoma.

TL;DR: The results revealed that novel crosstalk between KLF4 and ZEB1 regulated gemcitabine resistance in PDAC.
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Dysregulation of Krüppel-like factor 12 in the development of endometrial cancer.

TL;DR: This research reveals that overexpressed KLF12 contributes the growth of EC tumor by activating AKT signaling and increasing CCND1expression level and is expected to provide a novel potential therapeutic target for EC treatment.
References
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