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LSD1 mediates AKT activity in PIK3CA mutant colorectal cancer [ChIP-Seq]

ABSTRACT: LSD1 mediates AKT activity in PIK3CA mutant colorectal cancer [ChIP-Seq]

PROVIDER: PRJNA587643 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10400204.fastq.gz	Fastqsanger.gz
	SRR10400205.fastq.gz	Fastqsanger.gz
	SRR10400206.fastq.gz	Fastqsanger.gz
	SRR10400207.fastq.gz	Fastqsanger.gz
	SRR10400208.fastq.gz	Fastqsanger.gz

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LSD1 mediates AKT activity in PIK3CA mutant colorectal cancer [RNA-Seq]

Project description:Activation of the epithelial-mesenchymal transition (EMT) program is a critical mechanism for initiating cancer progression and migration. Colorectal cancers (CRCs) contain many genetic and epigenetic alterations that can contribute to EMT. Mutations activating the PI3K/AKT signaling pathway are observed in >40% of patients with CRC contributing to increased invasion and metastasis. Little is known about how oncogenic signaling pathways such as PI3K/AKT synergize with chromatin modifiers to activate the EMT program. Lysine Specific Demethylase 1 (LSD1) is a chromatin-modifying enzyme that is overexpressed in colorectal cancer (CRC) and enhances cell migration. In this study we determine that LSD1 expression is significantly elevated in CRC patients with mutation of the catalytic subunit of PI3K, PIK3CA, compared to CRC patients with WT PIK3CA. LSD1 enhances activation of the AKT kinase in CRC cells through a non-catalytic mechanism, acting as a scaffolding protein for the transcription-repressing CoREST complex. Additionally, growth of PIK3CA mutant CRC cells is uniquely dependent on LSD1. Knockdown or CRISPR knockout of LSD1 blocks AKT-mediated stabilization of the EMT-promoting transcription factor Snail and effectively blocks AKT-mediated EMT and migration. Overall we uniquely demonstrate that LSD1 mediates AKT activation in response to growth factors and oxidative stress, and LSD1-regulated AKT activity promotes EMT-like characteristics in a subset of PIK3CA mutant cells.

2019-11-06 | GSE139924 | GEO

LSD1 mediates AKT activity in PIK3CA mutant colorectal cancer [ChIP-Seq]

2019-11-06 | GSE139925 | GEO

LSD1 mediates AKT activity in PIK3CA mutant colorectal cancer

Project description:LSD1 mediates AKT activity in PIK3CA mutant colorectal cancer

| PRJNA587634 | ENA

LSD1 mediates AKT activity in PIK3CA mutant colorectal cancer [RNA-Seq]

Project description:LSD1 mediates AKT activity in PIK3CA mutant colorectal cancer [RNA-Seq]

| PRJNA587642 | ENA

LSD1 mediates AKT activity in PIK3CA mutant colorectal cancer

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

2019-11-06 | GSE139927 | GEO

Inhibition of PIK3CA by miR-203a-3p reduces hypertrophic scar formation via PI3K/AKT/mTOR signaling pathway

Project description:Hypertrophic scar (HS) is a skin fibroproliferative disease currently having no truly effective therapy. PIK3CA is a catalytic subunit of PI3K able to promote collagen synthesis in benign fibrotic diseases and to regulate cell survival, proliferation, and adhesion in malignancies. To explore PIK3CA’s functions in HS formation, we performed transcriptome sequencing and experimental validation. PIK3CA were overexpressed in HS tissues, and positively correlated with fibrosis. We then screened out miR-203a-3p as the most suitable endogenous inhibitor of PIK3CA through bioinformatics. Intriguingly, miR-203a-3p suppressed the proliferation, migration, collagen synthesis, and contractility, as well as trans-differentiation of fibroblasts into myofibroblasts in vitro, improved the morphology and histology of HS in vivo. Mechanistically, miR-203a-3p attenuated fibrosis by inactivating PI3K/AKT/mTOR pathway via directly targeting PIK3CA. In conclusion, Our findings identified that PIK3CA and PI3K/AKT/mTOR pathway were actively involved in HS formation and demonstrated that miR-203a-3p might serve as a potential strategy for HS therapy through targeting PIK3CA and inactivating PI3K/AKT/mTOR pathway.

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Expression data from Control, AKT and RAS transduced cells

Project description:Mutations in both RAS and the PTEN/PIK3CA/AKT signaling module are found in the same human tumors. PIK3CA and AKT are downstream effectors of RAS, and the selective advantage conferred by mutation of two genes in the same pathway is unclear. Based on a comparative molecular analysis, we show that activated PIK3CA/AKT is a weaker inducer of senescence than is activated RAS. More-over, concurrent activation of RAS and PIK3CA/AKT impairs RAS-induced senescence. We used microarrays to detail the global programme of gene expression after transduction of AKT and RAS IMR90 cells were transfected with Control, AKT and RAS retrovirus containing medium in 4 replicates. Fibroblasts were drug selected and kept in drug for duration of experiments.

2013-03-19 | E-GEOD-45276 | biostudies-arrayexpress

Expression data from Control, AKT and RAS transduced cells

2013-03-19 | GSE45276 | GEO

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