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Different forms of KLF5 transcriptionally regulate distinct sets of genes in prostate cancer cells [ChIP-Seq]

ABSTRACT: To identify which genes are directly regulated by KLF5 and its acetylation, we performed ChIP-Seq and bioinformatics analyses in KLF5-null prostate cancer cells expressing KLF5, KLF5KR, and KLF5KQ.

ORGANISM(S): Homo sapiens

PROVIDER: GSE161949 | GEO | 2020/12/19

REPOSITORIES: GEO

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Different forms of KLF5 regulate distinct sets of genes in prostate cancer cells [RNA-seq]

Project description:To identify which genes are regulated by KLF5 and its acetylation, we performed RNA-Seq and bioinformatics analyses in KLF5-null prostate cancer cells expressing KLF5, KLF5KR, and KLF5KQ.

2020-12-19 | GSE161950 | GEO

Different forms of KLF5 transcriptionally regulate distinct sets of genes in prostate cancer cells [ChIP-Seq]

Project description:Different forms of KLF5 transcriptionally regulate distinct sets of genes in prostate cancer cells [ChIP-Seq]

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Different forms of KLF5 regulate distinct sets of genes in prostate cancer cells

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Different forms of KLF5 regulate distinct sets of genes in prostate cancer cells

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

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Different forms of KLF5 regulate distinct sets of genes in prostate cancer cells [RNA-seq]

Project description:Different forms of KLF5 regulate distinct sets of genes in prostate cancer cells [RNA-seq]

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Interuption of Klf5 acetylaiton at K358 affects tumor microenvironment in Pten deficient mouse prostates

Project description:PTEN deficiency induces KLF5 acetylation; and the interruption of KLF5 acetylation orchestrates intricate interactions between cancer cells and CAFs that enhance FGFR1 signaling and promote tumor growth. Deacetylated KLF5 promotes tumor cells to secrete TNF, which stimulates inflammatory CAFs to release FGF9. Single-cell transcriptomic analysis reveals an enhanced FGF signaling from fibroblasts to cancer cells after the interruption of Klf5 acetylation.

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Expression data from conditional Klf5 knockout Pten-null mouse prostates

Project description:KLF5 is a basic transcription factor that regulates multiple biological processes, but its function in tumorigenesis appears contradictory in the current literature, with some studies showing tumor suppressor activity and others showing tumor promoting activity. In this study, we examined the function of Klf5 in prostatic tumorigenesis using mice with prostate specific deletion of Klf5 and Pten, both of which are frequently deleted in human prostate cancer. Histological and molecular analyses demonstrated that when one Pten allele was deleted, which causes mouse intraepithelial neoplasia (mPIN), Klf5 deletion accelerated the emergence and progression of mPIN. When both Pten alleles were deleted, which causes prostate cancer, Klf5 deletion promoted tumor growth and caused more severe morphological and molecular alterations, and homozygous deletion of Klf5 was more effective than hemizygous deletion. Unexpectedly, while Klf5 deletion clearly promoted tumorigenesis in luminal cells, it actually diminished the numbers of Ck5-positive basal cells in the Pten-null tumors. Klf5 deletion also increased the cell proliferation rate in tumors with Pten deletion, which involved extensive activation of the PI3K/AKT and MAPK mitogenic signaling pathways and inactivation of the p15 cell cycle inhibitor. Global gene expression and pathway analyses demonstrated that multiple mechanisms could be responsible for the tumor promoting effect of Klf5 deletion, We used microarrays to detail the global programme of gene expression of Klf5-wildtype and Klf5-null mouse dorsal prostates under Pten-null context to figure out the differential expression profiling underlying tumorigenesis 4 Klf5-wildtype and 4 Klf5-null mouse (6 months age) dorsal prostates under Pten-null context were used for RNA extraction and hybridization on Affymetrix mouse st 1.0 array

2014-06-21 | E-GEOD-58719 | biostudies-arrayexpress

Expression data from conditional Klf5 knockout Pten-null mouse prostates

2014-06-21 | GSE58719 | GEO

Interuption of Klf5 acetylaiton at K358 affects gene expression profiles in Pten deficient mouse prostates

Project description:Cancer associated fibroblasts (CAFs) play a pivotal role in tumor progression, but it remains elusive whether and how PTEN-deficient prostate cancers reprogram CAFs to overcome the barriers for tumor progression. Herein, we report that PTEN deficiency induces KLF5 acetylation; and interruption of KLF5 acetylation orchestrates intricate interactions between cancer cells and CAFs that enhance FGFR1 signaling and promote tumor growth. Deacetylated KLF5 promotes tumor cells to secrete TNF-α, which stimulates inflammatory CAFs to release FGF9. CX3CR1 inhibition blocks FGFR1 activation triggered by FGF9 and sensitizes PTEN-deficient prostate cancer to AKT inhibitor capivasertib.

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Over-expression and knockdown of KLF5

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