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Triptolide sensitizes cancer cells to nucleoside DNA methyltransferase inhibitors through inhibition of DCTPP1 mediated cell-intrinsic resistance

ABSTRACT: Triptolide sensitizes cancer cells to nucleoside DNA methyltransferase inhibitors through inhibition of DCTPP1 mediated cell-intrinsic resistance

PROVIDER: PRJNA770276 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16290087_1.fastq.gz	Fastqsanger.gz
	SRR16290087_2.fastq.gz	Fastqsanger.gz
	SRR16290088_1.fastq.gz	Fastqsanger.gz
	SRR16290088_2.fastq.gz	Fastqsanger.gz
	SRR16290089_1.fastq.gz	Fastqsanger.gz

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Triptolide sensitizes cancer cells to nucleoside DNA methyltransferase inhibitors through inhibition of DCTPP1 mediated cell-intrinsic resistance [Array]

Project description:We show that high DCTPP1 expression was associated with cell-intrinsic resistance to nucleoside DNMT inhibition, and that triptolide and its analogs could overcome this resistance.

2024-10-01 | GSE185594 | GEO

Triptolide sensitizes cancer cells to nucleoside DNA methyltransferase inhibitors through inhibition of DCTPP1 mediated cell-intrinsic resistance [RNA-Seq]

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Triptolide sensitizes cancer cells to nucleoside DNA methyltransferase inhibitors through inhibition of DCTPP1 mediated cell-intrinsic resistance [Array]

Project description:Triptolide sensitizes cancer cells to nucleoside DNA methyltransferase inhibitors through inhibition of DCTPP1 mediated cell-intrinsic resistance [Array]

| PRJNA769734 | ENA

Triptolide sensitizes cancer cells to nucleoside DNA methyltransferase inhibitors through inhibition of DCTPP1 mediated cell-intrinsic resistance [RNA-Seq]

Project description:Triptolide sensitizes cancer cells to nucleoside DNA methyltransferase inhibitors through inhibition of DCTPP1 mediated cell-intrinsic resistance [RNA-Seq]

| PRJNA770279 | ENA

Triptolide sensitizes cancer cells to nucleoside DNA methyltransferase inhibitors through inhibition of DCTPP1 mediated cell-intrinsic resistance

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

2024-10-01 | GSE185651 | GEO

Dysregulation of lncRNAs and circRNAs in mouse testes after exposure to triptolide

Project description:Triptolide has been shown to exert various pharmacological effects on systemic autoimmune diseases and cancers. However, its severe toxicity, especially reproduction toxicity, prevents wide clinical use for those people with fertility needs. Noncoding RNAs including lncRNAs and cicrRNAs are regulatory molecules that mediate a wide variety of physiological activities, which are critical for spermatogenesis, and their dysregulation might lead to male infertility. However, whether they are involved in triptolide-induced reproduction toxicity is fully unknown. Here, after exposure of mice to triptolide for 35 day, the total RNAs were used to investigate lncRNAs/cicrRNAs/mRNAs expression profiles by strand-specific RNA sequencing at the transcriptome level to help determine any RNA-related mechanisms in triptolide-induced toxicity. The results showed that triptolide significantly decreased the testicular weight, damaged testis and sperm morphology, reduced sperm motility and density. Furthermore, there's a remarkable deformity in sperm head and tail in triptolide-exposed mice. At the transcriptome level, the triptolide-treated mice exhibited aberrant expression profiles for lncRNAs/cicrRNAs/mRNAs, many of them were dysregulated. Gene ontology and pathway analyses revealed that the functions of differentially expressed lncRNA targets, cicrRNAs cognate genes and mRNAs were closely linked with many processes involved in spermatogenesis. Additionally, many newly identified lncRNAs /cicrRNAs displayed inducible expression, suggesting that they might be good candidate markers for triptolide-induced male reproductive toxicity. This study gives us an insight into understanding the reproductive system toxicity of triptolide and reminds us to strengthen the research on increasing efficacy and decreasing toxicity of triptolide.

2020-03-23 | GSE126857 | GEO

TIMELESS haploinsufficiency induces a PARG-dependency that is rescued by nucleoside supplementation, thus mimicking intrinsic PARG inhibitor sensitivity of ovarian cancer cells

Project description:A subset of cancer cells are intrinsically sensitive to inhibitors targeting PARG, the poly(ADP-ribose) glycohydrolase that degrades PAR chains. Sensitivity is accompanied by persistent DNA replication stress, and can be induced by inhibition of TIMELESS, a replisome accelerator. However, the nature of the oncogenic vulnerability responsible for intrinsic sensitivity remains undetermined. To understand PARG activity dependency, we analyzed Timeless model systems and intrinsically sensitive ovarian cancer cells. We show that nucleoside supplementation rescues all phenotypes associated with PARG inhibitor sensitivity, including replisome speed and fork-restart ability, S-phase completion and mitotic entry, proliferation dynamics and clonogenic potential, in both a TIMELESShaploinsufficient model and intrinsically sensitive cells. Importantly nucleoside supplementation restores PARG inhibitor resistance without reverting PAR chain accumulation, indicating that sensitivity correlates with PAR chain intolerance. We show that inhibition of thymidylate synthase, an enzyme required for dNTP homeostasis, induces PARG-dependency, and, using label-free, quantitative proteomics, we show that PKMYT1, a negative regulator of CDK1, is overexpressed in PARG inhibitor-sensitive cells. Together, these observations suggest that PARG inhibitor sensitivity reflects an inability to control replisome speed and/or maintain helicase-polymerase coupling in response to nucleotide imbalances, in turn applying selective pressure on mitotic entry controls to maintain genome integrity.

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The genes affected by Triptolide in activated mouse primary T cells

Project description:Triptolide possesses immunosuppressive activity and its efficacy is commonly believed to be related to the suppression of T cells. However, the underlying mechanism is still not well documented and most of the previous study adopted tumor cell lines of immune system as model cells in mechanism research, these cells’ signal transduction pathway can not reflect the real situation of immune system. In this study, we investigated the immunosuppressive mechanism of triptolide on T cell activation and proliferation using mouse primary T lymphocytes. These effects were analyzed along with activation of the TCR and AP-1 pathway. We used microarrays to detail the global programme of gene expression underlying stimulation and triptolide treatment. Mouse primary T cells stimulated with anti-CD3/CD28 antibodies treated with triptolide or not treated with triptolide were selected for RNA extraction and hybridization on Affymetrix microarrays.

2012-12-29 | E-GEOD-32315 | biostudies-arrayexpress

Expression data from treatment of actinomycin D and triptolide on MCF7 cells

Project description:Expression data from treatment of actinomycin D (2.5uM) and triptolide (500 nM) on MCF7 cells for 2, 4 and 6 hours. We used microarrays to explore the mechanism of triptolide action.

2011-10-18 | GSE28662 | GEO

Transcriptome of cancer associated fibroblasts before and after triptolide treatment in pancreatic cancer

Project description:Pancreatic cancer is characterized by heavy desmoplasia. Triptolide and its water-soluble pro-drug Minnelide are extremely efficient against pancreatic cancer in animal models. However, the effects of triptolide on pancreatic cancer stromal cells are largely unknown. The aim of this project is to indentify potential cellular functions that are affected by triptolide in pancreatic cancer associated fibroblasts.

2016-11-01 | GSE74490 | GEO

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