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Identification of transcripts induced after treatment with protein disulfide isomerase inhibitor E64FC65 and panobinostat in PANC-1 cells

ABSTRACT: Protein disulfide isomerase and histone deacetylase inhibition induces a synergistic pro-apoptotic response. The goal of this RNA-Seq experiment is to (1) identify critical transcripts and pathways induced by the combination in PANC-1 cells that promote apoptosis and (2) conduct RNA-seq in parallel with ATF3 knockdown to identify ATF3-dependent target genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE142210 | GEO | 2019/12/18

REPOSITORIES: GEO

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Identification of transcripts induced after treatment with protein disulfide isomerase inhibitor E64FC65 and panobinostat in PANC-1 cells

Project description:Identification of transcripts induced after treatment with protein disulfide isomerase inhibitor E64FC65 and panobinostat in PANC-1 cells

| PRJNA596223 | ENA

Expression data from SH-SY5Y neuroblastoma cells treated with the protein disulfide isomerase inhibitor origamicin

Project description:Protein disulfide isomerase (PDI) is associated with many diseases including neurodegenerative disorders like Alzheimer’s disease and, hence, is considered a promising drug target. In this study, we investigate the abscisic acid (ABA)-derived PDI inhibitor origamicin for its neuropharmacological potential. We used microarrays to analyze the global change in gene expression as a result of PDI inhibition in the human neuroblastoma cell line SH-SY5Y

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Treatment of Neuroblastoma Cells with Inhibitors of Protein Disulfide Isomerase Upregulates NQO1 Activity

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Protective Role for the Disulfide Isomerase PDIA3 in Methamphetamine Neurotoxicity

Project description:Methamphetamine abuse continues to be a worldwide problem, damaging the individual user as well as society. Only minimal information exists on molecular changes in the brain that result from methamphetamine administered in patterns typical of human abusers. In order to investigate such changes, we examined the effect of methamphetamine on the transcriptional profile in brains of monkeys. Gene expression profiling of the caudate and hippocampus identified protein disulfide isomerase family member A3 (PDIA3) to be significantly up-regulated in the animals treated with methamphetamine as compared to saline treated control monkeys. Treatment of primary rat neurons with methamphetamine revealed an up-regulation of PDIA3, showing a direct effect of methamphetamine on neurons to increase PDIA3. In vitro studies using a neuroblastoma cell line demonstrated that PDIA3 expression protects against methamphetamine-induced cell toxicity and methamphetamine-induced intracellular reactive oxygen species production, revealing a neuroprotective role for PDIA3. The current study implicates PDIA3 to be an important cellular neuroprotective mechanism against a toxic drug, and as a potential target for therapeutic investigations. To study the effects of chronic METH effects on the brain

2011-11-15 | E-GEOD-33707 | biostudies-arrayexpress

Therapeutic Targeting of Protein Disulfide Isomerase PDIA1 in Multiple Myeloma

Project description:Therapeutic Targeting of Protein Disulfide Isomerase PDIA1 in Multiple Myeloma

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Protective Role for the Disulfide Isomerase PDIA3 in Methamphetamine Neurotoxicity

2011-11-15 | GSE33707 | GEO

Treatment of Neuroblastoma Cells with Inhibitors of Protein Disulfide Isomerase Upregulates NQO1 Activity

Project description:Treatment of Neuroblastoma Cells with Inhibitors of Protein Disulfide Isomerase Upregulates NQO1 Activity

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Protein disulfide isomerase inhibition synergistically enhances the efficacy of sorafenib for hepatocellular carcinoma

Project description:Protein disulfide isomerase inhibition synergistically enhances the efficacy of sorafenib for hepatocellular carcinoma

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Protein disulfide isomerase inhibition synergistically enhances the efficacy of sorafenib for hepatocellular carcinoma [Hep3B]

Project description:Sorafenib is the only approved targeted drug for hepatocellular carcinoma (HCC), but its effect on patients’ survival gain is limited and varies over a wide range depending on patho-genetic conditions. Thus, enhancing the efficacy of sorafenib and finding a reliable predictive biomarker are crucuial to achieve efficient control of HCCs. In this study, we employed a systems approach by combining transcriptome analysis of the mRNA changes in HCC cell lines in response to sorafenib with network analysis to investigate the action and resistance mechanism of sorafenib. Gene ontology and gene set analysis revealed that proteotoxic stress and apoptosis modules are activated in the presence of sorafenib. Further analysis of the endoplasmic reticulum (ER) stress network model combined with in vitro experiments showed that introducing an additional stress by treating the orally active protein disulfide isomerase (PDI) inhibitor (PACMA 31) can synergistically increase the efficacy of sorafenib in vitro and in vivo, which was confirmed using a mouse xenograft model. We also found that HCC patients with high PDI expression show resistance to sorafenib and poor clinical outcomes, compared to the low PDI expression group. These results suggest that PDI is a promising therapeutic target for enhancing the efficacy of sorafenib and can also be a biomarker for predicting sorafenib responsiveness.

2017-03-19 | GSE96792 | GEO

Protein disulfide isomerase inhibition synergistically enhances the efficacy of sorafenib for hepatocellular carcinoma [Huh7]

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