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Cell cycle checkpoint proficiency of endometrial cancer cells

ABSTRACT: Cell cycle checkpoint proficiency of endometrial cancer cells

PROVIDER: PRJNA1040325 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26830900_1.fastq.gz	Fastqsanger.gz
	SRR26830900_2.fastq.gz	Fastqsanger.gz
	SRR26830901_1.fastq.gz	Fastqsanger.gz
	SRR26830901_2.fastq.gz	Fastqsanger.gz
	SRR26830904_1.fastq.gz	Fastqsanger.gz

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Cell cycle checkpoint proficiency of endometrial cancer cells [WES]

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Project description:Endometrial cancers (EC) are the most common gynecologic malignancy in the US. Most ECs harbor limited targetable somatic alterations, and are often grouped by histology (endometrioid, serous, or clear cell), mismatch repair, or TP53 status, none of which perfectly predict therapeutic response. A better mechanistic understanding of the key functional defects in ECs and more therapies with which to engage those targets in advanced stage EC are needed. Here we utilize functional, transcriptomic and genomic assays on a panel of EC cell lines and patient-derived organoids across EC histologic and genomic subtypes to characterize the TP53 and RB1 cell cycle regulatory proficiency and therapeutic vulnerabilities in this disease. We were surprised to find that TP53 genomic and functional status has little predictive capacity for EC therapeutic response. Rather, RB regulatory status correlated better with response to G1/S targeted therapies.

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

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Mre11 suppresses replication stress and gene amplification proficiency

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endometrial cancer

Project description:endometrial cancer with Bergen

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PEA15 regulates the DNA damage induced cell cycle checkpoint and oncogene-directed transformation

Project description:Regulation of the DNA damage response and cell cycle progression is critical for maintaining genome integrity. Here we report that in response to DNA damage, COPS5 deubiquitinates and stabilizes PEA15 in an ATM kinase-dependent manner. PEA15 expression oscillates throughout the cell cycle, and the loss of PEA15 accelerates cell cycle progression by activating CDK6 expression via the c-JUN transcription factor. Cells lacking PEA15 exhibit a DNA damage-induced G2/M checkpoint defect due to increased CDC25C activity and consequentially higher CDK1/Cyclin B activity and accordingly have an increased rate of spontaneous mutagenesis. We find that oncogenic RAS inhibits PEA15 expression and ectopic PEA15 expression blocks RAS-mediated transformation, which can be partially rescued by ectopic expression of CDK6. Finally, we show that PEA15 expression is down regulated in colon, breast and lung cancer samples. Collectively, our results demonstrate that tumor suppressor PEA15 is a regulator of genome integrity and is an integral component of the DNA damage response pathway that regulates cell cycle progression, the DNA-damage-induced G2/M checkpoint and cellular transformation. HCT116 cells stably expressing a non-silencing shRNA or two individual shRNAs against PEA15 were used to prepare the total RNA, which was then used to analyze for gene expression using Illumina expression array.

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