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To study the function of KLF5 in squamous cancers and gastrointestinal cancers [RNA-seq]

ABSTRACT: To identify KLF5 target genes and study the gene regulation function of KLF5 by integrating ChIP-seq, HiChIP and RNA-seq assays

ORGANISM(S): Homo sapiens

PROVIDER: GSE147855 | GEO | 2020/12/09

REPOSITORIES: GEO

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To study the function of KLF5 in squamous cancers and gastrointestinal cancers [HiChIP]

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Project description:This SuperSeries is composed of the SubSeries listed below.

2020-12-09 | GSE147856 | GEO

Inhibition of super enhancer downregulates the expression of KLF5 in basal-like breast cancers

Project description:The transcription factor KLF5 is highly expressed in basal-like breast cancer (BLBC). It promotes cell proliferation, survival, migration and stemness and serves as a potential therapeutic target. In this study, we first identified a super-enhancer (SE) located downstream of the KLF5 gene in BLBC. JQ-1, a BRD4-bromodomain inhibitor, inhibits the expression and activity of KLF5 in the HCC1806 and HCC1937 cell lines in time- and dose-dependent manners. A new BRD4 inhibitor, compound 870, is more potent than JQ-1 in terms of its ability to inhibit KLF5 and BLBC growth by inducing G1 phase cell cycle arrest. Additionally, a CDK7 inhibitor, THZ1, also inhibits KLF5 and BLBC growth. Our findings suggested that SE regulates KLF5 and that SE inhibitors could be an effective therapeutic strategy for treating BLBC.

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Genomic alterations activating KLF5 [RNA-Seq]

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KLF5 governs sphingolipid metabolism and barrier function of the skin

Project description:Stem cells are fundamental units of tissue remodeling, whose functions are dictated by lineage-specific transcription factors. Home to epidermal stem cells and their upward stratifying progenies, skin relies upon its secretory functions to form the outmost protective barrier, of which a transcriptional orchestrator has been elusive. KLF5 is a Krüppel-like transcription factor broadly involved in development and regeneration, whose lineage specificity, if any, remains unclear. Here we report KLF5 specifically marks the epidermis, and its deletion leads to skin barrier dysfunction in vivo. Lipid envelopes and secretory lamellar bodies are defective in KLF5-deficient skin, accompanied by preferential loss of complex sphingolipids. KLF5 binds to and transcriptionally regulates genes encoding rate-limiting sphingolipid metabolism enzymes. Remarkably, skin barrier defects elicited by KLF5 ablation can be rescued by dietary interventions. Finally, we found KLF5 is widely suppressed in human diseases with disrupted epidermal secretion, and its regulation of sphingolipid metabolism is conserved in human skin. Altogether, we establish KLF5 as a disease-relevant transcription factor governing sphingolipid metabolism and barrier function in the skin, likely representing a long-sought secretory lineage defining factor across tissue types.

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