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Triptolide Targets Super-Enhancer Networks in Pancreatic Cancer Cells and Cancer Associated Fibroblasts

ABSTRACT: Triptolide Targets Super-Enhancer Networks in Pancreatic Cancer Cells and Cancer Associated Fibroblasts

PROVIDER: PRJNA663345 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12638500.fastq.gz	Fastqsanger.gz
	SRR12638501.fastq.gz	Fastqsanger.gz
	SRR12638502.fastq.gz	Fastqsanger.gz
	SRR12638503.fastq.gz	Fastqsanger.gz
	SRR12638504.fastq.gz	Fastqsanger.gz

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Triptolide Targets Super-Enhancer Networks in Pancreatic Cancer Cells and Cancer Associated Fibroblasts

Project description:This study invesitgated the super-enhancer (SE) networks in pancreatic cancer cells and cancer associated fibroblasts (CAFs) as well as the effects of triptolide treatment on the SEs and the expression of the SE associated genes using ChIP-Seq and RNA-Seq.

2021-01-01 | GSE157927 | GEO

Triptolide targets super-enhancer networks in pancreatic cancer cells and cancer-associated fibroblasts.

Project description:The tumor microenvironment in pancreatic ductal adenocarcinoma (PDAC) is highly heterogeneous, fibrotic, and hypovascular, marked by extensive desmoplasia and maintained by the tumor cells, cancer-associated fibroblasts (CAFs) and other stromal cells. There is an urgent need to identify and develop treatment strategies that not only target the tumor cells but can also modulate the stromal cells. A growing number of studies implicate the role of regulatory DNA elements called super-enhancers (SE) in maintaining cell-type-specific gene expression networks in both normal and cancer cells. Using chromatin activation marks, we first mapped SE networks in pancreatic CAFs and epithelial tumor cells and found them to have distinct SE profiles. Next, we explored the role of triptolide (TPL), a natural compound with antitumor activity, in the context of modulating cell-type-specific SE signatures in PDAC. We found that TPL, cytotoxic to both pancreatic tumor cells and CAFs, disrupted SEs in a manner that resulted in the downregulation of SE-associated genes (e.g., BRD4, MYC, RNA Pol II, and Collagen 1) in both cell types at mRNA and protein levels. Our observations suggest that TPL acts as a SE interactive agent and may elicit its antitumor activity through SE disruption to re-program cellular cross talk and signaling in PDAC. Based on our findings, epigenetic reprogramming of transcriptional regulation using SE modulating compounds such as TPL may provide means for effective treatment options for pancreatic cancer patients.

| S-EPMC7653036 | biostudies-literature

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

Suppression of lung cancer development by aspirin and triptolide

Project description:Chronic inflammation plays important role in lung cancer development. Recently, we found that anti-inflammation drugs aspirin and triptolide when combined showed synergistic effect in suppressing lung cancer development. In this study, we aim to use gene microarray to define the genes and pathways that are affected by aspirin, triptolide individually or in combination.

2017-06-01 | GSE99514 | GEO

Triptolide analogs induced apoptosis on pancreatic cancer patient-derived organoids

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

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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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Triptolide analogs induced apoptosis on pancreatic cancer patient-derived organoids

Project description:Investigate the MOA of triptolide analog-CK21 in pancreatic cancer. Time course transcriptomic profiling of tumor organoids treated with CK21 in vitro revealed <10 differentially expressed genes (DEGs) at 3 h and ~8,000 DEGs at 12 h. Overall inhibition of general RNA transcription was observed, and Ingenuity pathway analysis together with functional cellular assays confirmed inhibition of the NF-κB pathway, increased oxidative phosphorylation and mitochondrial dysfunction, leading ultimately to increased reactive oxygen species (ROS) production, reduced B-cell-lymphoma protein 2 (BCL2) expression, and mitochondrial-mediated tumor cell apoptosis.

2023-11-24 | GSE225011 | 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

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

Analyses of mIRNA transcript level following exposure to triptolide

Project description:Analyses of mirna transcript levels following exposure to the drug triptolide in vitro and prodrug minnelide in xenograft pancreatic tumor mouse models. Response of pancreatic adenocarcinoma cell lines to minelide in vitro and exposure to its prodrug triptolide in SCID mouse tumors derived from the same cell lines.

2013-11-12 | E-GEOD-46188 | biostudies-arrayexpress

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