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BET inhibition induces synthetic lethality in BRCA2-deficient pancreatic cancer via autophagy-dependent cell death

ABSTRACT: BET inhibition induces synthetic lethality in BRCA2-deficient pancreatic cancer via autophagy-dependent cell death

PROVIDER: PRJNA854647 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19910417_1.fastq.gz	Fastqsanger.gz
	SRR19910417_2.fastq.gz	Fastqsanger.gz
	SRR19910418_1.fastq.gz	Fastqsanger.gz
	SRR19910418_2.fastq.gz	Fastqsanger.gz
	SRR19910419_1.fastq.gz	Fastqsanger.gz

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BET inhibition induces synthetic lethality in BRCA2-deficient pancreatic cancer via autophagy-dependent cell death [CUT&RUN]

Project description:BET inhibition induces synthetic lethality in BRCA2-deficient pancreatic cancer via autophagy-dependent cell death [CUT&RUN]

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BET inhibition induces synthetic lethality in BRCA2-deficient pancreatic cancer via autophagy-dependent cell death [RNA-Seq]

Project description:BET inhibition induces synthetic lethality in BRCA2-deficient pancreatic cancer via autophagy-dependent cell death [RNA-Seq]

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BET inhibition induces synthetic lethality in BRCA2-deficient pancreatic cancer via autophagy-dependent cell death [RNA-Seq]

Project description:To model familial pancreatic cancer patients, we generated isogenic Brca2 deficient pancreatic cancer cell lines with CRISPR/Cas9. To investigate the changes in the transcriptome profiles upon BET inhibition, we performed RNA-seq.

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BET inhibition induces synthetic lethality in BRCA2-deficient pancreatic cancer via autophagy-dependent cell death [CUT&RUN]

Project description:To model familial pancreatic cancer patients, we generated isogenic Brca2 deficient pancreatic cancer cell lines with CRISPR/Cas9. To investigate the changes in the enhancer landscape upon BET inhibition, we performed H3K27ac CUT-and-RUN-seq.

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BET inhibition induces synthetic lethality in BRCA2-deficient pancreatic cancer via autophagy-dependent cell death

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

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Gene expression of non-apoptotic pancreatic acinar cell death with autophagy

Project description:Serine protease inhibitor Kazal type 3 (Spink3) is a trypsin inhibitor in the pancreas. Spink3-/- pancreatic acinar cells are dead with excessive autophagy at birth (p0.5). To prove the role of nonapoptotic cell death with autophagy, we generated by transgenic technology the pancreas of Spink3-/-;XKI/+ mice contained both normal and dying acinar cells with autophagy. In this new mouse model, chronic inflammation occurred in the pancreas, indicating that some signals from nonapoptotic dead cell induce chronic inflammation in the pancreas. All samples were the pancreas at p0.5. Sample 1 and 2 are the pancreas from wild type (Spink3+/+, control) mice. Sample 3 and 4 are the pancreas from Spink3-/-, which all pancreatic acinar cells show induced nonapoptotic cell death with autophagy. Sample 5 and 6 are the pancreas from Spink3-/-XKI/+, about half acinar cells are normal, but other acinar cells show induced nonapoptotic cell death with autophagy.

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Nano gold simulated autophagy prevents cell death

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Transcription-Replication Conflicts drive the Synthetic Lethality of PARP Inhibitors with BRCA2-Deficiency

Project description:Transcription-Replication Conflicts drive the Synthetic Lethality of PARP Inhibitors with BRCA2-Deficiency

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Large-scale genetic screens identify BET-1 as a cytoskeleton regulator promoting actin health and lifespan

Project description:The actin cytoskeleton is a three-dimensional scaffold of proteins that is a regulatory, energy-consuming material with dynamic properties shaping the structure and function of the cell. The proper function of actin is required for many cellular pathways, including cell division, autophagy, chaperone function, endocytosis, and exocytosis (1–5). The breakdown of these cellular processes manifests during aging and exposure to stress, which is in part due to the breakdown of the actin cytoskeleton (5–9). However, the regulatory mechanisms involved in preservation of cytoskeletal form and function are not well understood. Here, we performed a multi-pronged, cross-organismal screen combining a whole-genome CRISPR-Cas9 screen in human fibroblasts with in vivo C. elegans synthetic lethality screening. We identified the bromodomain protein, BET-1, as a key regulator promoting actin health and longevity. Interestingly, overexpression of bet-1 preserves actin health at late age and promotes lifespan and healthspan in C. elegans. These beneficial effects are through preservation of actin, downstream of the function of BET-1 as a transcriptional regulator. Together, our discovery attributes assigns a key role of BET-1 in cytoskeletal health, highlighting regulatory cellular networks promoting cytoskeletal homeostasis.

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2023-06-01 | E-MTAB-11786 | biostudies-arrayexpress