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Reduced MEK inhibition confers a growth advantage and reduces genomic instability in naïve human ES cells (RNA-seq data set)

ABSTRACT: Reduced MEK inhibition confers a growth advantage and reduces genomic instability in naïve human ES cells (RNA-seq data set)

PROVIDER: PRJNA434588 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6748810_1.fastq.gz	Fastqsanger.gz
	SRR6748810_2.fastq.gz	Fastqsanger.gz
	SRR6748820_1.fastq.gz	Fastqsanger.gz
	SRR6748820_2.fastq.gz	Fastqsanger.gz
	SRR6748811_1.fastq.gz	Fastqsanger.gz

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Reduced MEK inhibition confers a growth advantage and reduces genomic instability in naïve human ES cells (RRBS-seq data set)

Project description:Human embryonic stem cells (hESCs) can be captured in either a primed state resembling the post-implantation epiblast or in a naïve state resembling the pre-implantation epiblast. Naïve culture conditions allow study of pre-implantation development ex vivo but reportedly lead to chromosomal abnormalities, compromising their utility in research and potential therapeutic applications. Although MEK inhibition is essential for the naïve state, here we show that reduced MEK inhibition facilitates the establishment and maintenance of naïve hESCs that retain naïve-specific transcriptional and DNA methylation patterns yet accrue fewer chromosomal abnormalities. We further show that hESCs cultured under these modified conditions are less prone to apoptosis and proliferate more rapidly. Our results point to the importance of residual MAPK signaling and provide a simple modification to current protocols to enable robust growth and genomic stability in naïve hESCs.

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Project description:Since gastric cancer (GC) is characterized by amplifications of receptor tyrosine kinases (RTK) and KRAS, targeting the RTK/KRAS downstream pathways could contribute to broader applicability of molecular targeted therapy in GC. Here, we assembled a panel of 49 GC cell lines and screened predictors for responsiveness to RAF/MEK/ERK pathway inhibition by comparing their sensitivity to MEK inhibition with alteration status of RTK/KRAS and phosphorylation status of RTK/KRAS downstream molecules. We found that GC cells with MET amplification or KRAS mutation tend to be sensitive to MEK inhibition. Furthermore, lower phosphorylation levels of mTORC1 targets, p70S6K and 4EBP1, was also significantly associated with sensitivity to MEK inhibition. Interestingly, the sensitive cells showed reduced mTORC1 activity accompanied by decreased rate of protein synthesis after MEK inhibition, suggesting that antiproliferative effect of MEK inhibition may be exerted through inhibition of protein synthesis, which was caused by reduced mTORC1 activity. Mechanistically, expression of some mTORC1 negative regulators, such as DDIT4, FOXO3, SESN1 and TSC1, were induced by MEK inhibition in highly-sensitive cell lines and knockdown of these negative regulators partially alleviated the suppression of mTORC1 activity and antiproliferative effect of MEK inhibition. Our data suggest that a subset of GCs, which would be distinguishable according to the predictive markers we identified, may be sensitive to MEK inhibition and have implications for the strategy in clinical trial of MEK inhibitors for GC.

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Reduced MEK inhibition preserves genomic stability in naïve human ES cells

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

2018-07-10 | GSE111020 | GEO

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Project description:Transcripts (mRNA) during amino acid limitation after MEK was inhibited were analyzed. HepG2 cells were pretreated with MEK inhibitor, PD98059 for 1 hour, then incubated in complete medium and a medium depleted for Histidine for 8 hours. For Inhibitor treated cells, PD98059 was included in the medium during the following 8 hours-incubation.

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