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Klf4 gene disruption is linked to enhanced cellular proliferation and tumor formation

ABSTRACT: Kruppel-like factor 4 (KLF4) is involved in diverse biological processes such as cell cycle control, differentiation, transcriptional regulation, DNA repair and apoptosis. Furthermore, KLF4 is a tumor suppressor and play a role in regulating genomic stability. In order to investigate the changes in gene expression in the klf4 null MEFs, we compared the gene expression patterns of the wild type and klf4 null by microarray. Total RNA isolated from Klf4 -/- MEFs compared to Klf4 +/+ MEFs. RNA was processed from cells that had reached 80-90 confluency in triplicate using Trizol reagent as recommended by the manufacturer (Invitrogen, Carlsbad, CA). RNA was subjected to DNase I treatment in order to remove any contaminating genomic DNA. Final purification was performed on RNAeasy columns (Qiagen, Valencia, CA), according to the manufacturer's recommendations.

ORGANISM(S): Mus musculus

SUBMITTER: Engda Hagos

PROVIDER: E-GEOD-21768 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Klf4 gene disruption is linked to enhanced cellular proliferation and tumor formation

Project description:Kruppel-like factor 4 (KLF4) is involved in diverse biological processes such as cell cycle control, differentiation, transcriptional regulation, DNA repair and apoptosis. Furthermore, KLF4 is a tumor suppressor and play a role in regulating genomic stability. In order to investigate the changes in gene expression in the klf4 null MEFs, we compared the gene expression patterns of the wild type and klf4 null by microarray.

2010-11-25 | GSE21768 | GEO

Identification of KLF4 regulated transcriptional features in breast cancer

Project description:Kruppel-like factor 4 (KLF4), as a eukaryotic transcription factor, participates in the regulation of cell proliferation, differentiation, embryonic development and other important life processes. KLF4 is also closely related to the occurrence and development in variety types of tumor. To determine the functions of KLF4 in breast cancer, we over-expressed KLF4 in breast cancer LM2-4175 cells and used gene expression profiling to identify KLF4 regulated genes.

2023-05-21 | GSE175844 | GEO

KLF4 binding is involved in the organization and regulation of 3D enhancer networks during acquisition and maintenance of pluripotency.

Project description:Cell fate transitions are accompanied by global transcriptional, epigenetic and topological changes driven by transcription factors (TFs), as is strikingly exemplified by reprogramming somatic cells to pluripotent stem cells (PSCs) via expression of OCT4, KLF4, SOX2 and cMYC. How TFs orchestrate the complex molecular changes around their target gene loci in a temporal manner remains incompletely understood. Here, using KLF4 as a paradigm, we provide the first TF-centric view of chromatin reorganization and its association to 3D enhancer rewiring and transcriptional changes of linked genes during reprogramming of mouse embryonic fibroblasts (MEFs) to PSCs. Inducible depletion of KLF factors in PSCs caused a genome-wide decrease in the connectivity of enhancers, while disruption of individual KLF4 binding sites from PSC-specific enhancers was sufficient to impair enhancer-promoter contacts and reduce expression of associated genes. Our study provides an integrative view of the complex activities of a lineage-specifying TF during a controlled cell fate transition and offers novel insights into the order and nature of molecular events that follow TF binding.

2019-09-03 | PXD014631 | Pride

KLF4 as a rheostat of osteolysis and osteogenesis in prostate tumors in the bone

Project description:We previously found that KLF4, a gene highly expressed in adult prostate stem cells, blocks the progression of indolent intraepithelial prostatic lesions into aggressive and rapidly growing tumors. To test whether this anti-cancer effect of KLF4 can also prevent prostate cancer-induced damage to the bone, we ablated KLF4 in human PC3 prostate cancer cells using CRISPR/Cas9-mediated genome editing and compared their behavior to null cells transduced with a DOX inducible KLF4 expression system. KLF4 re-expression inhibited growth of PC3 null cells in monolayer and as colonies in soft agar in a dose-dependent manner. When injected into the mouse femurs, PC3 null cells proliferated rapidly, forming very large, invasive and osteolytic tumors. Induction of KLF4 expression in PC3 null cells immediately after their intra-femoral inoculation blocked the development of tumors while preserving the normal bone architecture. KLF4 re-expression in established PC3 bone tumors inhibited osteolytic effects of PC3 null cells, preventing bone fractures and inducing a significant osteogenic response with regions of new bone formation. Transcriptome analyses of PC3 cells with no or high KLF4 expression revealed KLF4-dependent osteolytic or osteogenic transcriptional programs, respectively. Importantly, these KLF4-dependent functions significantly overlapped with metastatic prostate cancers in patients.

2019-05-09 | GSE117965 | GEO

Gene expression in reprogramming MEF fractions FACS-sorted by Oct4, Klf4 and EpCAM expression

Project description:After 8 days of OKSM induction via doxycycline, Nanog-Neo secondary MEFs (Wernig et al. Nature Biotechnology 2008) were FACS sorted by KLF4, Oct4, and EpCAM expression. Four major subsets of MEFs have been sorted and analysed for gene expression.

2014-08-01 | GSE56764 | GEO

Gene expression in reprogramming MEF fractions FACS-sorted by Oct4, Klf4 and EpCAM expression

2014-08-01 | E-GEOD-56764 | biostudies-arrayexpress

Klf4 expression in conventional dendritic cells is required for T helper 2 cell responses

Project description:Subset-specific and progenitor gene expression analysis of Klf4+/+ and Klf4-/- DCs. The two major lineages of classical dendritic cells (cDCs) express and require either IRF8 or IRF4 transcription factors for their development and function. IRF8-dependent cDCs promote anti-viral and T-helper 1 (Th1) cell responses, whereas IRF4-expressing cDCs have been implicated in controlling both Th2 and Th17 cell responses. Here, we have provided evidence that Kruppel-like factor 4 (Klf4) is required in IRF4-expressing cDCs to promote Th2 but not Th17 cell responses in vivo. Conditional Klf4 deletion within cDCs impaired Th2 cell responses during Schistosoma mansoni infection, Schistosoma egg antigen (SEA) immunization, and house dust mite challenge (HDM), without affecting cytotoxic T lymphocyte (CTL), Th1 and Th17 cell responses to herpes simplex virus, Toxoplasma gondii and Citrobacter rodentium infections. Further, Klf4 deletion reduced IRF4 expression in pre-cDCs and resulted in selective loss of IRF4-expressing cDCs subsets in several tissues. These results indicate that Klf4 guides a transcriptional program promoting IRF4-expressing cDCs heterogeneity.

2015-05-19 | GSE68590 | GEO

Klf4 expression in conventional dendritic cells is required for T helper 2 cell responses

2015-05-19 | E-GEOD-68590 | biostudies-arrayexpress

Transcriptome Data of KLF4 Overexpression in Human Umbilical Vein Endothelial Cells

Project description:Atheroprotective flow (e.g., pulsatile shear stress) and statins drastically induce the expression of krüppel-like factor 4 (KLF4) in vascular endothelial cells (ECs). We therefore investigated the role of KLF4 in EC function through comparing the transciptional profiling of human umbilical vein endothelial cells (HUVECs) that were infected with adenovirus overexpression KLF4 (Ad-KLF4) or with empty vector (Ad-null) control. Gene ontology analysis revealed that KLF4 not only regulates EC homeostasis through the upregulation of nitric oxide synthesis and vascular development, but also mediates response to lipid. Among the lipid responsive genes, KLF4 exhibited induction of cholesterol efflux and oxidation [i.e., liver X receptor (LXR) and cholesterol 25-hydroxylase (Ch25h)], while suppressing cholesterol biosynthesis [i.e., sterol regulatory element-binding protein 2 (SREBP2)].

2017-10-05 | GSE90982 | GEO

Klf4

Project description:Klf4 is the zinc finger transcription factor indispensable for terminal maturation of epithelial tissues and part of group of proteins for the generation of pluripotent embryonic stem cells from differentiated tissues. No definitive in-vivo-function of Klf4 in the hematopoietic system has been established yet. We show here that Klf4 directly guides the transcriptional program for terminal differentiation of Ly-6Chigh monocytes. Klf4 suppresses transcripts of the interferon immune response and induces a proinflammatory cytokine transcriptional program. Concordantly, Klf4 hematopoietic deficiency in mice results in an enhanced Th1 but impaired Th17 immune response, and, consequently, those mice are resistant towards the induction of experimental autoimmune encephalitis (EAE). We here identify Klf4 is a transcription factor required for ontogenesis and function of Ly-6Chigh monocytes at the interface of innate and acquired immunity.

2012-07-31 | GSE11572 | GEO

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