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UPR induction in samples derived from OVCAR5 cancer cells treated with spirocyclic dimer SpiD7

ABSTRACT: UPR induction in samples derived from OVCAR5 cancer cells treated with spirocyclic dimer SpiD7

PROVIDER: PRJNA786885 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17156316.fastq.gz	Fastqsanger.gz
	SRR17156316_1.fastq.gz	Fastqsanger.gz
	SRR17156316_2.fastq.gz	Fastqsanger.gz
	SRR17156317.fastq.gz	Fastqsanger.gz
	SRR17156317_1.fastq.gz	Fastqsanger.gz

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UPR induction in samples derived from OVCAR5 cancer cells treated with spirocyclic dimer SpiD7

Project description:The objective of this study was to evaluate the transcriptional changes in OVCAR5 cells upon treatment with a spirocyclic α-methylene-γ-butyrolactone dimer SpiD7. To assess if SpiD7 activates Unfolded Protein Response, OVCAR5 cells were treated with SpiD7 for different time points. A time dependent increase in the expression of genes in the hallmark UPR gene set was observed demonstrating induction of UPR.

2021-12-10 | GSE190368 | GEO

Spirocyclic dimer (SpiD7) activates unfolded protein response (UPR) to selectively inhibit growth and induce apoptosis of cancer cells

Project description:Protein homeostasis is maintained by a combination of tightly controlled processes which include synthesis, folding, trafficking and degradation. Transient accumulation of unfolded / misfolded proteins in the endoplasmic reticulum (ER) due to cell intrinsic and / or extrinsic signals results in the activation of unfolded protein response (UPR), an adaptation mechanism. Failure to resolve the transient accumulation results in UPR mediated programmed cell death. Loss of tumor suppressor gene or oncogene addiction in cancer cells result in a sustained higher basal UPR levels. This higher basal UPR levels in cancer cells when compared to normal cells provides a therapeutic window that can be exploited by UPR activators. Here we explored covalent modification of surface exposed cysteine (SEC) residues to simulate unfolded / misfolded proteins and induce UPR activation. A proteome-wide click-pulldown-MS study using an alkyne tagged isatin-derived spirocyclic -methylene--butyrolactone analog identified > 330 protein targets that were covalently modified. Evaluation for UPR activation with a set of analogs that can covalently modify SECs identified a spirocyclic -methylene--butyrolactone dimer (SpiD7) as a UPR activator. SpiD7 induced XBP1 splicing protected normal cells from caspase-mediated apoptosis, no such induction was observed in cancer cells, which resulted in caspase-mediated apoptosis in cancer cells. SpiD7 inhibits growth of high-grade serous carcinoma (HGSC) cell lines ~3-15 fold more potently than immortalized fallopian tube epithelial (normal) cells and reduced clonogenic growth of HGSC cell lines. Our results suggest that induction of UPR by covalent modification of SEC residues is a cancer cell vulnerability and can be exploited to discover novel therapeutics.

2022-05-20 | PXD029783 | Pride

RNA Sequencing Analysis of Human Ovarian Cancer Cell Line OVCAR5 Treated with Stearic Acid, Oleic Acid, and CAY10566

Project description:This study investigates the anti-proliferative effects of long chain fatty acids on cancer cells, focusing on the specific impacts of oleate and stearate. We explored how these fatty acids, prevalent in biological systems, influence cellular processes. Our analysis revealed that the top 10 significantly upregulated Gene Ontology (GO) categories in OVCAR5 cells treated with 50 µM stearate (compared to control cells) are enriched in pathways related to the unfolded protein response (UPR) and endoplasmic reticulum (ER) stress.

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Genome-wide maps of H3K79Me3 binding sites in ovarian cancer cell line OVCAR5 and expression profile of DOT1L knockdown OVCAR5 cells (ChIP-seq)

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Genome-wide maps of H3K79Me3 binding sites in ovarian cancer cell line OVCAR5 and expression profile of DOT1L knockdown OVCAR5 cells (RNA-seq)

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Project description:This study characterized the genome-wide binding of FOXK2 in ovarian cancer (OC) cell OVCAR-5 and investigated the expression profile of OVCAR5 cells with FOXK2 knocking-down.

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Genome-wide maps of FOXK2 binding sites in ovarian cancer cell line OVCAR5 and expression profile of FOXK2 knockdown OVCAR5 cells (RNA-seq)

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