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

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

PROVIDER: PRJEB29293 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2854350_1.fastq.gz	Fastqsanger.gz
	ERR2854350_2.fastq.gz	Fastqsanger.gz
	ERR2854341_1.fastq.gz	Fastqsanger.gz
	ERR2854341_2.fastq.gz	Fastqsanger.gz
	ERR2854351_1.fastq.gz	Fastqsanger.gz

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

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Gene expression profile of multiple myeloma cell lines treated with CB-5083

Project description:The goal was to determine the gene expression differences between CB-5083 and Bortezomib treated multiple myeloma cell lines Inhibition of the AAA ATPase, p97, was recently shown to be a novel method for targeting the ubiquitin proteasome system (UPS) and CB-5083, a first in class inhibitor of p97, has demonstrated broad antitumor activity in a range of both hematological and solid tumor models. Here, we show that CB-5083 has robust activity against multiple myeloma (MM) cell lines and a number of in vivo MM models. Treatment with CB-5083 is associated with accumulation of ubiquitinated proteins, induction of the unfolded protein response (UPR) and apoptosis. CB-5083 decreases viability in MM cell lines and patient derived MM cells, including those with background proteasome inhibitor (PI) resistance. CB-5083 has a unique mechanism of action that combines well with PIs which is likely owing to the p97-dependent retro-translocation of the transcription factor, Nrf1, which transcribes proteasome subunit genes following exposure to a PI. In vivo studies using clinically relevant MM models demonstrate that single-agent CB-5083 inhibits tumor growth and combines well with MM standard of care agents. Our preclinical data demonstrate the efficacy of CB-5083 in several MM disease models and provide the rationale for clinical evaluation as monotherapy and in combination in MM.

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HCT116 cells treated with the p97 inhibitior CB-5083

Project description:The goal of this study was to analyze differential gene expression 8 hr after treatment of CB-5083, a small molecule inhibitor of p97 (VCP), in HCT116 cells grown in culture. DMSO treated cells were compared to cells treated with 1uM CB-5083 after 8 hr.

2015-11-09 | E-GEOD-73588 | biostudies-arrayexpress

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Project description:The goal of this study was to analyze differential gene expression 8 hr after treatment of CB-5083, a small molecule inhibitor of p97 (VCP), in HCT116 cells grown in culture.

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Project description:MOLM-13 acute myeloid leukemia cells were treated with 7 µM 5-Azacytidine (Cayman Chemical 11164), or 450 nM CB-5083 (Cayman Chemical 19311), or in combination, or 0.1% DMSO as control. Treatments were conducted for 48 hours.

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Effect of inhibition of VCP on gene expression during colorectal cancer progression of HCT116 cells

Project description:To investigate the signaling patheway of VCP regulation PD-L1 in colorectal cancer cells, HCT116 cells were treated with CB-5083. We then performed gene expression profiling analysis using data obtained from RNA-seq of 3 different cells CB-5083 treatment and untreatment.

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human ovarian cancer cells:parental PTX-sensitive cells (OVCAR-3) vs. PTX-resistant cells (OV3R-PTX)

Project description:Transcriptional profiling (lncRNA and mRNA) of human ovarian cancer cells comparing parental PTX-sensitive cells (OVCAR-3) vs. PTX-resistant cells (OV3R-PTX, derived from OVCAR-3).

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Project description:Oxaliplatin resistance was induced in 2 colorectal cancer cell lines (LoVo-92, wt-p53 and LoVo-Li, functionally inactive p53) and one ovarian cancer cell line (A2780, wt-p53). Resistance was induced by weekly exposure to oxaliplatin for 4 hrs or 72 hrs with increasing concentrations for a period of 7 months Genomic DNA of oxaliplatin and cisplatin resistant colorectal cancer and ovarian cancer cell lines as well as the parental cell lines were labeled and subsequently hybridized against pooled reference DNA of healthy volunteers of the opposite gender using across array hybridization. Extracted raw-data were normalised and smoothend using the R-script NOWAVE resulting in normalised log2 ratio profiles of resistant cell line versus parental cell line and parental cell line versus reference DNA.

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