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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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Beyond proliferation: KLF5 promotes angiogenesis of bladder cancer through directly regulating VEGFA transcription

TL;DR: It is found that KLF5 was essential for cancer cell-endothelial cell interaction in vitro and tumor angiogenesis in nude mice based on lentivirus-mediated KLf5 knockdown bladder cancer cell models and two pivotal pathways in bladder cancer, RTKs/RAS/MAPK and PI3K/Akt, might convey their oncogenic signaling through KLF 5-VEGFA axis.
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miR-145-5p affects the differentiation of gastric cancer by targeting KLF5 directly.

TL;DR: The role of miR-145-5p/Kruppel-like factor 5 (KLF5) in the pathologic processes of many types of cancer remains unknown as mentioned in this paper.
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The deubiquitinase USP10 regulates KLF4 stability and suppresses lung tumorigenesis.

TL;DR: It is demonstrated that USP10 is a critical regulator of KLF4, pinpointing USP 10-KLF4-TIMP3 axis as a promising therapeutic target in lung cancer.
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ID1 Mediates Escape from TGFβ Tumor Suppression in Pancreatic Cancer.

TL;DR: PDAs that develop with the TGF-β pathway intact avert this apoptotic effect via Inhibitor of Differentiation 1 (ID1), which is identified as a crucial node and potential therapeutic target in PDA.
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APTO-253 Stabilizes G-quadruplex DNA, Inhibits MYC Expression, and Induces DNA Damage in Acute Myeloid Leukemia Cells.

TL;DR: The effect of APTO-253 on MYC expression and its downstream target genes, on cell-cycle arrest, DNA damage, and stress responses can be explained by the action of Fe(253)3 and APTO -253 on G-quadruplex DNA motifs.
References
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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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