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Pattern occupation of HDACs on chromatin determines PI3K/AKT inhibitor resistance in cancers [ChIP-seq]

ABSTRACT: Pattern occupation of HDACs on chromatin determines PI3K/AKT inhibitor resistance in cancers [ChIP-seq]

PROVIDER: PRJNA564807 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10095573_1.fastq.gz	Fastqsanger.gz
	SRR10095573_2.fastq.gz	Fastqsanger.gz
	SRR10095574_1.fastq.gz	Fastqsanger.gz
	SRR10095574_2.fastq.gz	Fastqsanger.gz
	SRR10095575_1.fastq.gz	Fastqsanger.gz

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Pattern occupation of HDACs on chromatin determines PI3K/AKT inhibitor resistance in cancers [ChIP-seq]

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Pattern occupation of HDACs on chromatin determines PI3K/AKT inhibitor resistance in cancers [RNA-seq]

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Project description:Pattern occupation of HDACs on chromatin determines PI3K/AKT inhibitor resistance in cancers [RNA-seq]

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An epigenetic vulnerability in PI3K/AKT inhibition resistant cancers is targetable by both bromodomain and HDAC inhibitors

Project description:Acquisition of resistance to PI3K/AKT-targeted monotherapy regardless of cancer types implies the existence of common mechanisms. Here we demonstrate that while causing glycolysis crisis, acetyl-CoA shortage and global decrease of histone acetylation, PI3K/AKT inhibitors induce drug resistance by selectively augmenting CBP/p300, H3K27 acetylation and BRD4 binding at genomic loci of a subset of growth factor and receptor (GF/R) genes. BRD4 occupation at these loci and drug resistant cell growth are vulnerable to both bromodomain and HDAC inhibitors. Little or none occupation of HDACs at the GF/R gene loci underscores the paradox that cells respond equivalently to the two classes of inhibitors with opposite modes of action. Targeting this unique epigenetic vulnerability offers a general solution to overcome PI3K/AKT inhibitor resistance in different cancers.

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Modulation of glutamine metabolism by the PI3K-PKB/c-akt-FOXO network regulates autophagy

Project description:This SuperSeries is composed of the following subset Series: GSE35701: CP001: Modulation of glutamine metabolism by the PI3K-PKB/c-akt-FOXO network regulates autophagy GSE35703: CP003: Modulation of glutamine metabolism by the PI3K-PKB/c-akt-FOXO network regulates autophagy Refer to individual Series

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FOXO3a Is A Major Target Of Inactivation By PI3K/AKT Signaling In Aggressive Neuroblastoma

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Transcription profiling of transgenic mice constitutively active for caPI3K and dominant-negative forms of PI3K (dnPI3K) to test if the insulin/IGF-IRS-PI3K-Akt determines organ size in vertebrates

Project description:The insulin/IGF-IRS-PI3K-Akt pathway is highly conserved in evolution. To test whether this signaling cascade determines organ size in vertebrates, we have recently created mouse lines transgenic for constitutively active (caPI3K) and dominant-negative forms of PI3K (dnPI3K) (Shioi et al., 2000). Transgene expression is driven by the cardiac-specific a -myosin heavy chain (MHC) promoter. Both transgenic lines are characterized by moderate but highly consistent changes in heart size, despite the fact that body weight and the size of other organs are completely normal. caPI3K transgenic animals have hearts 20% larger than those of wild type littermates, whereas dnPI3K mice have hearts that are 17% smaller. The observed changes in heart size correlate with an appropriate increase or decrease in the size of transgenic cardiomyocytes. These hearts do not have cardiomyopathic changes, since the contractile function of transgenic hearts is normal, and signs of necrosis, apoptosis, or interstitial fibrosis are absent (see Physiology). These data suggest an autonomous role for PI3K in cell size regulation. Our goal is now to determine how activation of this system translates into changes in cell size by identifying the trigger and components of this signaling cascade. Heterozygous caPI3K (constitutively active PI3K) and dnPI3K (dominant-negative PI3K) transgenic female mice (5-14 months) compared with non-transgenic littermates. Transgene expression driven by the a -myosin heavy chain (a -MHC) promoter.

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PI3K/AKT pathway is activated by miRNA-22 in the proliferative CLL subset (mRNA)

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