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Proteotoxic stress-induced apoptosis in cancer cells: understanding the susceptibility and enhancing the potency

ABSTRACT: Proteotoxic stress-induced apoptosis in cancer cells: understanding the susceptibility and enhancing the potency

PROVIDER: PRJNA846688 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19571463_1.fastq.gz	Fastqsanger.gz
	SRR19571463_2.fastq.gz	Fastqsanger.gz
	SRR19571464_1.fastq.gz	Fastqsanger.gz
	SRR19571464_2.fastq.gz	Fastqsanger.gz
	SRR19571466_1.fastq.gz	Fastqsanger.gz

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Proteotoxic stress-induced apoptosis in cancer cells: understanding the susceptibility and enhancing the potency

Project description:Leiomyosarcoma (LMS) is an aggressive cancer with few therapeutic options. LMS cells are more sensitive to proteotoxic stress compared to normal smooth muscle cells. We used small compound 2c to induce proteotoxic stress and compare the transcriptomic adaptations of immortalized human uterine smooth muscle cells (HUtSMC) and LMS cells SK-UT-1. We found that the expression of the heat shock proteins (HSP) gene family is upregulated with higher efficiency in normal cells. In contrast, upregulation of BH3-only proteins is higher in LMS cells. HSF1, the master regulator of HSP transcription, is sequestered into transcriptionally incompetent nuclear foci only in LMS cells, which explains the lower HSP upregulation. We also found that several compounds can enhance the cell death response to proteotoxic stress. Specifically, when low doses were used, an inhibitor of salt-inducible kinases (SIKs) and the inhibitor of IRE1, a key element of the unfolded protein response (UPR), support proteotoxic-induced cell death with strength in LMS cells and without effects on the survival of normal cells. Overall, our data provide an explanation for the higher susceptibility of LMS cells to proteotoxic stress and suggest a potential option for co-treatment strategies.

2022-10-03 | GSE205596 | GEO

Proteotoxic stress-induced apoptosis in cancer cells: understanding the susceptibility and enhancing the potency.

Project description:Leiomyosarcoma (LMS) is aggressive cancer with few therapeutic options. LMS cells are more sensitive to proteotoxic stress compared to normal smooth muscle cells. We used small compound 2c to induce proteotoxic stress and compare the transcriptomic adaptations of immortalized human uterine smooth muscle cells (HUtSMC) and LMS cells SK-UT-1. We found that the expression of the heat shock proteins (HSPs) gene family is upregulated with higher efficiency in normal cells. In contrast, the upregulation of BH3-only proteins is higher in LMS cells. HSF1, the master regulator of HSP transcription, is sequestered into transcriptionally incompetent nuclear foci only in LMS cells, which explains the lower HSP upregulation. We also found that several compounds can enhance the cell death response to proteotoxic stress. Specifically, when low doses were used, an inhibitor of salt-inducible kinases (SIKs) and the inhibitor of IRE1α, a key element of the unfolded protein response (UPR), support proteotoxic-induced cell death with strength in LMS cells and without effects on the survival of normal cells. Overall, our data provide an explanation for the higher susceptibility of LMS cells to proteotoxic stress and suggest a potential option for co-treatment strategies.

| S-EPMC9531228 | biostudies-literature

Enhancing the Potency of Mouse Embryonic Stem Cells

Project description:Enhancing the Potency of Mouse Embryonic Stem Cells

| PRJNA388649 | ENA

Highly specific immunoproteasome inhibitor M3258 induces proteotoxic stress and apoptosis in MLL-AF4-driven acute lymphoblastic leukemia.

Project description:Proteasome inhibitors (PIs) Bortezomib, Carfilzomib and Ixazomib are approved for the treatment of multiple myeloma and mantle cell lymphoma and have clinical activity in acute lymphoblastic leukemia (ALL). The predominant form of proteasome in these hematologic malignancies is the lymphoid tissue specific immunoproteasome. FDA-approved PIs inhibit immunoproteasomes and ubiquitously expressed constitutive proteasomes causing on-target toxicities in non-hematological tissues. Replacing PIs with selective immunoproteasome inhibitors (IPIs) should reduce these toxicities. We have previously shown that IPI ONX-0914 causes apoptosis of ALL cells expressing the MLL-AF4 fusion protein but did not elucidate the mechanism. Here we show that a novel, highly specific IPI M3258 induces rapid apoptosis in ALL cells in vitro and is comparable to bortezomib in its ability to reduce tumor growth and enhance effect of chemotherapy in vivo. Treatment of ALL cells with M3258, ONX-0914 and bortezomib induced proteotoxic stress that was prevented by the protein synthesis inhibitor cycloheximide, which dramatically desensitized cells to PI-induced apoptosis. Thus, like MM, ALL cells are sensitive to PIs and IPIs because they are under proteotoxic stress caused by elevated rates of protein synthesis.

2025-04-10 | GSE282470 | GEO

RNA-seq: WT under proteotoxic stress conditions

Project description:In order to elucidate on mRNA changes upon various proteotoxic stress conditions, synchronized WT (N2) worms were treated from L4 to day 1 of adulthood and collected for RNA extraction in the following

2019-01-01 | GSE124178 | GEO

Enhancing the Potency of Mouse Embryonic Stem Cells [RNA-Seq]

Project description:Mouse naïve pluripotent stem cells (ESC) can contribute to all embryonic tissues and the germline, but rarely to the extra-embryonic tissues in chimeric embryos. Here we describe a novel advanced pluripotent stem cell (ASC) with higher potency, since a single ASC contributes very efficiently to the fetus, germline, yolk sac and the placental labyrinth in chimeras. ASCs were derived from blastocysts in two steps in a chemically defined medium with Activin A (ActA) and basic fibroblast growth factor (bFGF), followed by Wnt and BMP. Notably, ASCs exhibit a distinct transcriptome with the expression of both naïve pluripotent genes, as well as mesodermal somatic genes; Eomes, Eras, Tdgf1, Evx1, hand1, Wnt5a, and distinct repetitive elements. Established ESCs can also be readily and directly to ASCs. Importantly, ASCs exhibit a stable hypermethylated epigenome unlike the hypomethylated epiblast in blastocysts and naïve ESCs, indicating that ASCs might represent a state in between the naïve and primed states of pluripotency.

2017-11-01 | GSE99491 | GEO

Enhancing the Potency of Mouse Embryonic Stem Cells [BS-Seq]

2017-11-01 | GSE99488 | GEO

RNA-seq: WT under proteotoxic stress conditions

Project description:RNA-seq: WT under proteotoxic stress conditions

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Differentiational potency of induced pluripotent stem cells into cardiomyocytes

Project description:Transcriptional profiling of mouse induced pluripotent stem (iPS) cells with the low potency (strain 20D17) compared to control iPS cells with the normal potency (strain 38C2). Two-condition experiment: iPS cells strain 20D17 vs. control iPS cells strain 38C2. Biological replicates: 2 strain 20D17, 2 strain 38C2, independently grown and harvested. One replicate per array.

2010-06-23 | E-GEOD-18117 | biostudies-arrayexpress

Effect of peroxisomal proteotoxic stress on gene expression in mammalian cells

Project description:To establish the overall cell responses to peroxisomal proteotoxic stress, we analysed transcriptomes of NT- and LONP2-silenced cells using RNA sequencing in COS-7 and U2OS cells.

2023-09-27 | GSE224992 | GEO

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