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E-MTAB-7328

ABSTRACT: RNA-seq of human ovarian cancer cell line OVSAHO parental and CB-5083-resistant cells

PROVIDER: E-MTAB-7328 | ExpressionAtlas | 2025-01-23

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-MTAB-7328-analysis-methods.tsv	Tabular
	E-MTAB-7328-analytics.tsv	Tabular
	E-MTAB-7328-atlasExperimentSummary.Rdata	Rdata
	E-MTAB-7328-configuration.xml	Xml
	E-MTAB-7328-g3_g1-mvaPlot.png	Other

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RNA-seq of human ovarian cancer cell line OVSAHO parental and CB-5083-resistant cells

Project description:RNA-seq of human ovarian cancer cell line OVSAHO parental and CB-5083-resistant cells

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RNA-seq of human ovarian cancer cell line OVSAHO parental and CB-5083-resistant cells

Project description:The goal of this experiment is to identify differentially expressed genes between parental OVSAHO cells and CB-5083-resistant OVSAHO cells. Each group is treated with 5 microM CB-5083 for 6 hours and total RNA was extracted with Trizol. RNA sequencing library was performed using Illumina RNA library kit.

2018-11-02 | E-MTAB-7328 | biostudies-arrayexpress

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Project description:ATP-competitive p97 inhibitor CB-5339, the successor of CB-5083, is being evaluated in Phase 1 clinical trials for anti-cancer therapy. Different modes of action p97 inhibitors such as allosteric inhibitors are useful to overcome one the major problems of targeted therapy: drug-induced resistance. We previously demonstrated allosteric p97 inhibitor NMS-873 can overcome CB-5083-induced resistance. Here, we found that NMS-873 but not CB-5083 affected glycometabolism. By establishing NMS-873-resistant cell lines and performing both cell-based and proteomic analysis, we confirmed that NMS-873 dysregulates glycometabolism in a p97-independent manner. We then used proteome integral solubility alteration with a temperature-based method (PISA T) to identify NDUFAF5 as one of the potential targets of NMS-873 in the mitochondrial complex I. Overall, we employed chemical proteomics and drug-induced thermal proteome changes to identify drug targets, in combination with drug-resistant cell lines to dissect on- and off-target effects. We also demonstrated that glycolysis inhibitor 2-DG enhanced the anti-proliferative effect of NMS-873. The polypharmacology of NMS-873 can be advantageous for anti-cancer therapy.

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