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Transcriptome analysis of HeLa cells treated with the CDC7-specific inhibitor TAK-931 [RNA-seq]

ABSTRACT: The results showed that 48-h treatment upregulated 138 genes and 72-h treatment upregulated 504 genes. In the Metascape analyses, the TNF signaling pathway was a dominant network module in the 48-h treatment group, while the inflammatory-related modules were more intensively accumulated, and the signaling networks expanded to the surrounding various modules in the 72-h treatment. Our signaling module results indicate that the TAK-931-induced cellular senescence progressed in a time-dependent manner, and mTOR pathways plays important roles in viability for TAK-931-induced senescent cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE245063 | GEO | 2023/11/05

REPOSITORIES: GEO

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Transcriptome analysis of J558 allograft mouse model treated with the CDC7-specific inhibitor TAK-931 [RNA-seq]

Project description:To comprehensively evaluate in vivo inflammatory effects of TAK-931 in tumor microenvironment, RNA-seq was conducted in the J558 allograft mouse model. The GSEA revealed significant enrichment of inflammatory hallmarks in TAK-931-treated allografts. Metascape analyses also visualized that the network modules of the inflammatory signaling pathways were predominantly enriched.

2023-11-05 | GSE244988 | GEO

Gene expression profile at single cell level of HeLa cells treated with the CDC7-specific inhibitor TAK-931 [scRNA-seq]

Project description:We performed scRNA-seq analyses to determine the transcriptional landscape of the TAK-931-induced aneuploid cells at the single-cell levels. HeLa cells were treated with DMSO or TAK-931 (300 nM) for 72 h. In the t-SNE plots, the DMSO- and TAK-931-treated cells were classified in two distinct clusters. Indicating that the major population of the TAK-931-treated aneuploid HeLa cells was transformed to a cell contexture that was transcriptionally distinct from that of DMSO-treated control cells. The hallmark of an inflammatory response was remarkably enriched in the TAK-931 treatment cluster. In addition, the positive cells of inflammatory cytokine/chemokine-related genes, such as CXCL8, IL1B, TNHSF14 and TNFRSF1B, were significantly accumulated in the TAK-931-treatment cluster.

2023-11-05 | GSE244987 | GEO

Gene expression profile at single cell level of J558 allograft mouse model treated with the CDC7-specific inhibitor TAK-931 [scRNA-seq]

Project description:To comprehensively evaluate in vivo inflammatory effects of TAK-931 in tumor microenvironment, scRNA-seq was conducted in the J558 allograft mouse model. The tSNE plots and the expression dot plots showed cellular components in the allografts classified by the indicated TME markers: cancer cell (J558 allograft), monocyte, CD8+ T cell, CD4+ T cell, NK cell, endothelial cell, fibroblast, and undefined, demonstrating that TAK-931 treatment prominently promoted tumor infiltration of both adaptive (CD8+ T cell and CD4+ T cell) and innate (NK cells and monocytes) immune cells in the allografts.

2023-11-05 | GSE244986 | GEO

A Study to Evaluate the Safety, Tolerability, and Activity of TAK-931 in Participants With Metastatic Pancreatic Cancer, Metastatic Colorectal Cancer, and Other Advanced Solid Tumors

Project description:The purpose of this study is to confirm the safety and tolerability of TAK-931 in a cohort of Western participants with metastatic solid tumors and to evaluate the anti-tumor activity of TAK-931 in participants with metastatic pancreatic cancer, colorectal cancer (CRC), squamous esophageal cancer (sqEC), and squamous non-small-cell lung cancer (sqNSCLC).

| 2252731 | ecrin-mdr-crc

Actinonin induced changes in gene expression profiles in MEFs

Project description:Retrograde signaling induced remodelling of nuclear gene expression from mitochondrial ribosomal dysfunction was analyzed. Global expression profile changes in mouse embryonic fibroblasts were assesed under actinonin treatment 6, 24, 48 and 72 hours post drug addiction.

2013-07-05 | GSE44109 | GEO

Multi-level Support Vector Regression analysis to identify condition-specific regulatory networks

Project description:The identification of gene regulatory modules is an important yet challenging problem in computational biology. While many computational methods have been proposed to identify regulatory modules, their initial success is largely compromised by a high rate of false positives, especially when applied to human cancer studies. New strategies are needed for reliable regulatory module identification. We present a new approach, namely multi-level support vector regression (ml-SVR), to systematically identify conditionspecific regulatory modules. The approach is built upon a multi-level analysis strategy designed for suppressing false positive predictions. With this strategy, a regulatory module becomes ever more significant as more relevant gene sets are formed at finer levels. At each level, a two-stage support vector regression (SVR) method is utilized to help reduce false positive predictions by integrating binding motif information and gene expression data; a significant analysis procedure is followed to assess the significance of each regulatory module. We applied our method to breast cancer cell line data to identify condition-specific regulatory modules associated with estrogen treatment. Experimental results show that our method can identify biologically meaningful regulatory modules related to estrogen signaling and action in breast cancer.

2010-03-10 | GSE20700 | GEO

Multi-level Support Vector Regression analysis to identify condition-specific regulatory networks

2010-03-23 | E-GEOD-20700 | biostudies-arrayexpress

Cdk8, Cyclin C, Med12 or Med13 depletion effect on gene expression in Drosophila S2 cells

Project description:Expression profiling following depletion of Mediator Cdk8 module subunits Cdk8, Cyclin C (CycC), Med12 and Med13 72 hours after dsRNA treatment of Drosophila melanogaster S2 cells. Results provide insight into the role of individual Cdk8 module subunits in regulation of transcription.

2014-04-29 | GSE52343 | GEO

Targeting Pancreatic Cancer by TAK-981, a SUMOylation Inhibitor that Activates the Immune System and Blocks Cancer Cell Cycle Progression in a Preclinical Model

Project description:Pancreatic ductal adenocarcinoma (PDAC) has the characteristics of high-density desmoplastic stroma, a distinctive immunosuppressive microenvironment and is profoundly resistant to all forms of chemo and immunotherapy, leading to a 5-year survival rate of 9%. Our study aims to add novel small molecule therapeutics for the treatment of PDAC. We have studied whether TAK-981, a novel highly selective and potent small molecule inhibitor of the SUMO activating enzyme E1 (SAE) could be used to treat a preclinical syngeneic PDAC mouse model. We found that SUMOylation, a reversible post-translational modification required for cell cycle progression, is increased in PDAC patient samples compared to normal pancreatic tissue. TAK-981 decreased SUMOylation in PDAC cells at the nanomolar range, thereby causing a G2/M cell cycle arrest, mitotic failure and chromosomal segregation defects. TAK-981 efficiently limited tumor burden in the KPC3 syngeneic mouse model without evidence of systemic toxicity. In vivo treatment with TAK-981 enhanced the proportions of activated CD8 T cells and NK cells but transiently decreased B cell numbers in peripheral blood, spleen and lymph nodes. ScRNA sequencing revealed activation of the interferon response upon TAK-981 treatment in lymphocytes including T, B and NK cells. TAK-981 treatment of CD8 T cells ex vivo induced activation of STAT1 and interferon target genes. Our findings indicate that pharmacological inhibition of the SUMO pathway represents a potential strategy to target PDAC via a dual mechanism: inhibiting cancer cell cycle progression and activating anti-tumor immunity by inducing interferon signaling.

2022-01-11 | GSE189576 | GEO

A Study of TAK-186 (Also Known as MVC-101) in Adults With Advanced or Metastatic Cancer

Project description:The main aim of this study is to check for side effects and tolerability of TAK-186 (also known as MVC-101) in adults with unremovable advanced or metastatic cancer. Another aim is to characterize and evaluate the activity of TAK-186 (MVC-101). Participants may receive treatment throughout the study for a maximum of 13 months and will be followed up at 30 days and then every 12 weeks for up to 48 weeks after the last treatment.

| 2374243 | ecrin-mdr-crc

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