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Synthetic lethal CRISPR screen identifies a cancer cell-intrinsic role of PD-L1 in regulation of vulnerability to ferroptosis [CRISPR screening]

ABSTRACT: Synthetic lethal CRISPR screen identifies a cancer cell-intrinsic role of PD-L1 in regulation of vulnerability to ferroptosis [CRISPR screening]

PROVIDER: PRJNA1117744 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29535110_1.fastq.gz	Fastqsanger.gz
	SRR29535110_2.fastq.gz	Fastqsanger.gz
	SRR29535111_1.fastq.gz	Fastqsanger.gz
	SRR29535111_2.fastq.gz	Fastqsanger.gz

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Synthetic lethal CRISPR screen identifies a cancer cell-intrinsic role of PD-L1 in regulation of vulnerability to ferroptosis.

Project description:Synthetic lethal CRISPR screen identifies a cancer cell-intrinsic role of PD-L1 in regulation of vulnerability to ferroptosis.

| PRJNA1125334 | ENA

Synthetic lethal CRISPR screen identifies a cancer cell-intrinsic role of PD-L1 in regulation of vulnerability to ferroptosis [CUT&Tag]

Project description:Synthetic lethal CRISPR screen identifies a cancer cell-intrinsic role of PD-L1 in regulation of vulnerability to ferroptosis [CUT&Tag]

| PRJNA1117746 | ENA

Synthetic lethal CRISPR screen identifies a cancer cell-intrinsic role of PD-L1 in regulation of vulnerability to ferroptosis [CRISPR screening]

Project description:Despite the remarkable success of programmed death 1/PD-L1 inhibition in tumor therapy, only a minority of patients benefits from it. Previous studies suggest the anti-PD-1 treatment failure may attribute to the intrinsic functions of PD-L1 in cancer cells. Here, we established a genome-wide CRISPR synthetic lethality screen to systematic explore the PD-L1 intrinsic function in head and neck squamous cell carcinoma (HNSCC) cells. Ferroptosis related genes were identified to be essential for PD-L1 deficient cell viability. Genetic and pharmacological induction of ferroptosis accelerated cell death in PD-L1 knockout cells. PD-L1 knockout cells were also highly susceptible to immunogenic ferroptosis in vitro and in vivo. Mechanistically, nuclear PD-L1 transcriptionally activated SOD2 expression to maintain redox homeostasis. Importantly, the lower ROS and ferroptosis were observed in HNSCC patients with the higher expression of PD-L1. In summary, our study illustrates that PD-L1 confers ferroptosis resistance by activating SOD2-meidated redox homeostasis in HNSCC cells, indicating an enhanced therapeutic effect can be achieved by targeting the intrinsic PD-L1 function during immunotherapy.

2024-07-08 | GSE268533 | GEO

Synthetic lethal CRISPR screen identifies a cancer cell-intrinsic role of PD-L1 in regulation of vulnerability to ferroptosis [CUT&Tag]

2024-07-08 | GSE268534 | GEO

Synthetic lethal CRISPR screen identifies a cancer cell-intrinsic role of PD-L1 in regulation of vulnerability to ferroptosis.

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2024-07-05 | GSE270147 | GEO

Tumor cell-intrinsic Decr2 regulates ferroptosis and immunotherapy efficacy

Project description:Increased or decreased B16 cell sensitivity to activated cytotoxic T lymphocytes.To identify tumor cell-intrinsic genes essential for antigen-specific CD8+ T cell killing, we utilized the B16.SIY melanoma cell line which expressed the model antigen SIY (SIYRYYGL) co-expressed with DsRed, that can be recognized by 2C CD8+ TCR transgenic (Tg) T cells. B16.SIY cells were transduced and selected to stably expressed a Cas9 gene, and then transduced with a genome-scale CRISPR gRNA library.Transduced cells were cultured for 8 days to provide time for gene disruption to occur, then were co-cultured with pre-activated 2C CD8+ T cells at a 2:1 Effector:Target ratio for 16 hours. By performing deep sequencing, we examined the sgRNA library representation in tumor cells with or without T cell co-incubation by MAGeCK analysis.

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CHD1 is a synthetic lethal vulnerability in MYC-driven breast cancer

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Progressive Senescence Programs Elicit Intrinsic Vulnerability to Ageing-related Cancer

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Molidustat Targets a Synthetic Lethal Vulnerability in APC-Mutant Colorectal Cancer through GSTP1 and PHD2 Co-Inhibition

Project description:APC mutations drive colorectal cancer (CRC) and create dependencies on metabolic and stress-adaptation pathways. To investigate vulnerabilities associated with hydroxylase inhibition in APC-mutant cells, we profiled the proteomic consequences of the clinical PHD2 inhibitor Molidustat using thermal proteome profiling and chemical proteomics. These analyses revealed GSTP1 as an unexpected off-target interactor whose enzymatic activity is directly inhibited by Molidustat. Quantitative proteomics of CRISPR knockout models showed that loss of GSTP1 and PHD2 individually induces partially overlapping stress responses, whereas combined loss produces a synergistic redox-collapse phenotype, characterised by oxidative stress, apoptotic signalling, and impaired proliferation, closely recapitulating the cellular response to Molidustat. Metabolomics confirmed elevated oxidative pressure and altered redox balance in the double knockout. In parallel, Molidustat selectively reduced viability in APC- and KRAS-mutant colonic organoids, an effect not reproduced by other hydroxylase inhibitors. Together, these data identify a GSTP1–PHD2 synthetic lethal interaction and demonstrate that Molidustat exploits this vulnerability, providing a mechanistic basis for its selective activity in APC-mutant CRC.

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CHD1 is a synthetic lethal vulnerability in MYC-driven breast cancer [ATAC-seq]

Project description:CHD1 is a synthetic lethal vulnerability in MYC-driven breast cancer [ATAC-seq]

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