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Metabolic dependency mapping identifies Peroxiredoxin 1 as a driver of resistance to ATM inhibition

ABSTRACT: Metabolic dependency mapping identifies Peroxiredoxin 1 as a driver of resistance to ATM inhibition

PROVIDER: PRJNA1135133 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29804919_1.fastq.gz	Fastqsanger.gz
	SRR29804919_2.fastq.gz	Fastqsanger.gz
	SRR29804920_1.fastq.gz	Fastqsanger.gz
	SRR29804920_2.fastq.gz	Fastqsanger.gz
	SRR29804921_1.fastq.gz	Fastqsanger.gz

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Metabolic dependency mapping identifies Peroxiredoxin 1 as a driver of resistance to ATM inhibition

Project description:Metabolic pathways fuel tumor progression and resistance to stress conditions including chemotherapeutic drugs, such as DNA damage response (DDR) inhibitors. Yet, significant gaps persist in how metabolic pathways confer resistance to DDR inhibition in cancer cells. Here, we employed a metabolism-focused CRISPR knockout screen and identified genetic vulnerabilities to DDR inhibitors. We unveiled Peroxiredoxin 1 (PRDX1) as a synthetic lethality partner with Ataxia Telangiectasia Mutated (ATM) kinase. Tumor cells depleted of PRDX1 displayed heightened sensitivity to ATM inhibition in vitro and in mice in a manner dependent on p53 status. Mechanistically, we discovered that the ribosomal protein RPL32 undergoes redox modification on active cysteine residues 91 and 96 upon ATM inhibition, promoting p53 stability and altered cell fitness. Our findings reveal a new pathway whereby RPL32 senses stress and induces p53 activation impairing tumor cell survival.

2025-01-19 | GSE272107 | GEO

Metabolic dependency mapping identifies Peroxiredoxin 1 as a driver of resistance to ATM inhibition.

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Mapping Replication Stress-Dependent Transcriptional Events Dependent on ATM or ATMIN by RNA-seq

Project description:The cellular response to replication stress requires the DNA-damage responsive kinase ATM and its co-factor ATMIN, however the roles of this signaling pathway following replication stress are unclear. RNA-seq and subsequent differential expression analyses were utilized to identify the functions of ATM and ATMIN in response to replication stress induced by Aphidcolin (APH). Mouse Embryonic Fibroblasts (MEFs) deleted for ATM or ATMIN were treated with 1ÂµM APH or DMSO as a control. Two different wild-type MEF cell lines (wtATM, wtATMIN) served as controls. RNA-seq was performed in duplicates, in a total of 32 samples, with an average of 31.1M aligned readsobtained per group,with 15.5M reads obtained per replicate.

2016-04-14 | E-GEOD-72275 | biostudies-arrayexpress

Mapping Replication Stress-Dependent Transcriptional Events Dependent on ATM or ATMIN by RNA-seq

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Panicum virgatum strain:ATM | cultivar:ATM

Project description:Panicum virgatum ATM Resequencing genome sequencing

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Project description:LC-MS/MS data from swab sampling of ATM keypad buttons and finger tips of a person who typed a four-digit PIN.

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MiRNAs expression data from Atm++ and Atm-- mouse embryonic fibroblasts after DNA damage at various time point

Project description:Atm++ and Atm-- mouse embryonic fibroblasts were treated with DNA damaging agent neocarzinostatin (NCS), and cells were harvested at indicated time points for the microarray analyses of whole-genome miRNAs. To examine how miRNAs are regulated in the DNA damage response, we assessed the genome-wide mature miRNA expression in Atm++ and Atm-- littermate mouse embryonic fibroblasts (MEFs).

2010-12-20 | E-TABM-1092 | biostudies-arrayexpress

MiRNAs expression data from Atm+/+ and Atm-/- mouse embryonic fibroblasts after DNA damage at various time point

Project description:Atm+/+ and Atm-/- mouse embryonic fibroblasts were treated with DNA damaging agent neocarzinostatin (NCS), and cells were harvested at indicated time points for the microarray analyses of whole-genome miRNAs. To examine how miRNAs are regulated in the DNA damage response, we assessed the genome-wide mature miRNA expression in Atm+/+ and Atm-/- littermate mouse embryonic fibroblasts (MEFs).

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ATM Loss and Therapeutic Vulnerabilities in Bladder Cancer

Project description:ATM plays a central role in the cellular response to DNA damage and ATM alterations are common in several tumor types including bladder cancer. However, the specific impact of ATM alterations on therapy response in bladder cancer is uncertain. Here, we combine preclinical modeling and clinical analyses to comprehensively define the impact of ATM alterations in bladder cancer. We show that ATM loss is sufficient to increase sensitivity to DNA damaging agents including cisplatin and radiation. Furthermore, ATM loss drives sensitivity to DNA repair targeted agents including PARP and ATR inhibitors. ATM loss alters the immune microenvironment and improves anti-PD1 response in preclinical bladder models but is not associated with improved anti-PD1/PD-L1 response in clinical cohorts. Finally, we show that ATM expression by IHC is strongly correlated with response to chemoradiotherapy. Together these data define a potential role for ATM as a predictive biomarker in bladder cancer.

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