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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.

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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

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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]

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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]

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

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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.

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