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Krüppel-like Transcription Factor-10 (KLF10) Provides a Negative Feedback Mechanism to Suppress TGFβ-Induced Epithelial-to-Mesenchymal Transition [RNA-Seq]

ABSTRACT: We examined transcriptome-wide effects of pertrurbation in KLF10 function (siKLF10) on TGFβ-regulated genes and EMT in two different cells lines: A549 and Panc1.

ORGANISM(S): Homo sapiens

PROVIDER: GSE90566 | GEO | 2017/03/14

SECONDARY ACCESSION(S): PRJNA355089

REPOSITORIES: GEO

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Krüppel-like Transcription Factor-10 (KLF10) Provides a Negative Feedback Mechanism to Suppress TGFβ-Induced Epithelial-to-Mesenchymal Transition [ChIP-Seq]

Project description:We have elucidated the potential role of KLF10 in inhbiting TGFβ-induced EMT. Further, we show that KLF10 directly binds to SNAI2 and recruit HDAC1 to inhbit the expression of SNAI2.

2017-03-14 | GSE90565 | GEO

Krüppel-like Transcription Factor-10 (KLF10) Provides a Negative Feedback Mechanism to Suppress TGFβ-Induced Epithelial-to-Mesenchymal Transition

Project description:Krüppel-like Transcription Factor-10 (KLF10) Provides a Negative Feedback Mechanism to Suppress TGFβ-Induced Epithelial-to-Mesenchymal Transition

| PRJNA355088 | ENA

Krüppel-like Transcription Factor-10 (KLF10) Provides a Negative Feedback Mechanism to Suppress TGFβ-Induced Epithelial-to-Mesenchymal Transition

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

2017-03-14 | GSE90567 | GEO

Murine Pancreatic Cancer Cells: KLF10 wild type vs KLF10 knockout

Project description:Transcriptional profiling of mouse pancreatic cancer cells comparing Pdx-1Cre LSL-KrasG12D P53L/L cells with Pdx-1Cre LSL-KrasG12D KLF10L/L P53L/L cells, and to determine the effects of KLF10 deficiency on murine PDAC gene expression. Two-condition experiment, Pdx-1Cre LSL-KrasG12D P53L/L cells vs. Pdx-1Cre LSL-KrasG12D KLF10L/L P53L/L cells: 3 KLF10 wild type replicates, 3 KLF10 knockout replicates.

2016-08-22 | E-GEOD-85521 | biostudies-arrayexpress

KLF10 targets

Project description:Experiment comparing the liver transcriptome from wild type and KLF10 deficient mice

2010-04-19 | E-MEXP-2089 | biostudies-arrayexpress

Murine Pancreatic Cancer Cells: KLF10 wild type vs KLF10 knockout

2016-08-22 | GSE85521 | GEO

KLF10 modulates stem cell phenotypes of pancreatic adenocarcinoma by transcriptionally regulating notch receptors

Project description:KrÜppel-like factor 10 (KLF10), deficient in two thirds of 105 resected pancreatic adenocarcinoma (PDAC) patients, was associated with rapid loco-regional recurrence and large tumor size. Additional KLF10 depletion in KC (LSL: KrasG12D; Pdx1-CRE) mice accelerated progression from pancreatic intraepithelial neoplasia to PDAC. In Panc-1 cells with KLF10 deficiency (Panc-1-pLKO-shKLF10), increased sphere formation, stem cell markers expression, and tumor growth were noted compared with those of control. Over-expressing KLF10 genetically or pharmacologically using metformin, reversed the stem cell phenotypes induced by KLF10 depletion. Ingenuity pathway analysis and gene set enrichment analysis showed Notch signal molecules including Notch receptors 3 and 4 were over-expressed in Panc-1-pLKO-shKLF10. KLF10 transcriptionally suppressed Notch 3 and 4 receptors by competing with ELF3, a positive regulator, for promoter binding. Downregulating Notch signal genetically or pharmacologically ameliorated stem cell phenotypes of Panc-1-pLKO-shKLF10. Elevating KLF10 expression by metformin with concomitant evodiamine, a non-toxic Notch 3 methylation stimulator, delayed murine tumor growth of PDAC with KLF10 deficiency without prominent toxicity. These results demonstrated a novel signal pathway of KLF10 in modulating stem cell phenotypes of PDAC via transcriptional regulating Notch signal pathway. Elevating KLF10 and suppressing Notch signal may cooperatively reduce PDAC tumorigenesis and malignant progression.

2023-06-21 | GSE218172 | GEO

KLF10 promotes nonalcoholic steatohepatitis progression through transcriptional activation of zDHHC7 [KFL10 overexpression]

Project description:Nonalcoholic steatohepatitis (NASH), characterized by hepatic steatosis, inflammation, and liver injury, has become a leading cause of end-stage liver diseases and liver transplantation. Krüppel-like factors 10 (KLF10) is a Cys2/His2 zinc finger transcription factor that regulates cell growth, apoptosis, and differentiation. However, whether it plays a role in the development and progression of chronic liver diseases like NASH remains poorly understood. In the present study, we found that KLF10 expression was selectively upregulated in the mouse models and human patients with NASH, compared with simple steatosis (NAFL). Gain- and loss-of function studies demonstrated that hepatocyte-specific overexpression of KLF10 aggravated, whereas its depletion alleviated diet-induced NASH pathogenesis in mice. Mechanistically, transcriptomic analysis and subsequent functional experiments showed that KLF10 promotes hepatic lipid accumulation and inflammation through the palmitoylation and plasma membrane localization of fatty acid translocase CD36 via transcriptionally activation of zDHHC7. Indeed, both expression of zDHHC7 and palmitoylation of CD36 are required for the pathogenic roles of KLF10 in NASH progression. Thus, our results identify an important role for KLF10 in NAFL-to-NASH development through zDHHC7-mediated CD36 palmitoylation.

2022-02-25 | GSE197054 | GEO

KLF10 promotes nonalcoholic steatohepatitis progression through transcriptional activation of zDHHC7 [NAFL vs NASH]

2022-02-25 | GSE197053 | GEO

FOXO1-KLF10 reinforcing loop promotes adipose lipolysis to facilitate exercise-induced anti-obesity effect in male mice

Project description:Exercise is recognized to be an effective way in the combat against obesity and related metabolic disorders, but the underlying mechanism is incompletely understood. Krüppel-like factor 10 (KLF10) is a transcription factor participating in diverse biological processes. KLF10 expression is abundant in adipose tissue, but its role in obesity is not well defined. Here, we show that exercise could facilitate adipocyte-derived KLF10 expression via the SIRT1/FOXO1 pathway. Adipocyte-specific knockout of KLF10 (KLF10AKO) blunts exercise-promoted white adipose browning, energy expenditure, fat loss, and glucose tolerance in diet-induced obese (DIO) mice. On the contrary, adipocyte-specific transgenic expression of KLF10 in mice (KLF10ATG) enhanced the abovementioned metabolic benefits induced by exercise. Mechanistically, KLF10 interacts with FOXO1 and facilitates the recruitment of KDM4A to form a ternary complex on the promoter regions of the Pnpla2 and Lipe genes to promote the expression of these key lipolytic genes, therefore facilitating lipolysis to defend against DIO in mice. As a newfound downstream effector responding to exercise, adipose KLF10 could act as a potential target in the fight against obesity

2024-08-25 | GSE269020 | GEO

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