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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE185650 | GEO | 2024/10/01

REPOSITORIES: GEO

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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

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

| PRJNA770276 | ENA

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

Triptolide analogs induced apoptosis on pancreatic cancer patient-derived organoids

Project description:Triptolide analogs induced apoptosis on pancreatic cancer patient-derived organoids

| PRJNA933573 | ENA

Triptolide clears Staphylococcus aureus infection by targeting XIAP to induce host apoptosis while preserving gut microbiota homeostasis [iBDMDs]

Project description:Staphylococcus aureus (SA) remains a global health threat due to its increasing drug resistance and intracellular persistence, which compromise the efficacy of conventional antibiotics. Host-directed therapy (HDT) has emerged as a promising alternative by modulating host immunity. With the multi-targeting and immunomodulatory properties, Traditional Chinese Medicine (TCM) monomers represent ideal candidates for HDT. However, their ability to promote host immunity-mediated SA clearance remains largely unexplored. Here, we identified triptolide as a compound that facilitates intracellular clearance of SA and MRSA. Mechanistic studies revealed that triptolide directly binds to the X‑linked inhibitor of apoptosis protein (XIAP) to inhibit XIAP-caspase interaction, thereby releasing caspase inhibition and inducing apoptosis. Moreover, treatment with triptolide reduced bacterial loads and alleviated lung inflammation in mice infected with SA and MRSA, concurrently maintaining microbiota homeostasis and improving metabolic function. Taken together, these findings establish triptolide as a promising lead compound for the development of HDT against SA and MRSA infections.

2026-05-18 | PXD074476 | Pride

Triptolide clears Staphylococcus aureus infection by targeting XIAP to induce host apoptosis while preserving gut microbiota homeostasis [Mouse lung macrophages]

2026-05-18 | PXD074740 | Pride

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

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

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