Project description:This study was designed to evaluate the transcriptomic alterations upon SRMS deficiency after cisplatin exposure in a human ovarian cancer cell line.

2023-06-07 | GSE206226 | GEO

Differentially expressed genes upon TbSAC3 depletion

Project description:This study examines differential expression upon TbSAC3 depletion in Trypanosoma brucei brucei strain 29.13

2023-02-22 | GSE79773 | GEO

Dynamic response of annexin A11-associated gene expression to cisplatin treatment

Project description:Based on a time-course study of cisplatin response in ovarian cancer cells with/without suppression of annexin A11 expression using whole genome oligonucleotide microarrays, we identified a set of differentially expressed genes associated with annexin A11 expression and patterns of gene expressions in response to cisplatin exposure. Keywords: human ovarian cancer cell lines 2008 cells (one ovarian cancer cell line) were transfected with ANXA11_RNAi or control_RNAi for 2 days and then treated with 10 ÂµM cisplatin (Sigma) for 0, 8, 16, 24 hours. Total RNA of 8 samples were prepared for gene expression profiling using the Agilent 44K whole genome oligonucleotide microarrays.

2010-04-08 | E-GEOD-13893 | biostudies-arrayexpress

The M1 aminopeptidase NPEPPS is a novel regulator of cisplatin sensitivity

Project description:Platinum-based chemotherapeutics are used in many combination regimens in cancer. Despite extensive use across diverse cancer types, there is room for improved efficacy and patient selection for treatment. Here, we use bladder cancer to address both issues. A multi-omic assessment of five human bladder cancer cell lines and their chemotherapy resistant derivatives, coupled with in vitro whole-genome CRISPR screens were used to define functional drivers of treatment resistance. We identified 46 genes that sensitized the resistant cell lines to cisplatin plus gemcitabine (GemCis), a standard combination therapy in bladder cancer. Most genes were involved with DNA damage and repair pathways, which have previously been associated with enhanced sensitivity to cisplatin. Evaluating expression of the 46 genes in the whole transcriptome and proteome data in parental and resistant lines identified the puromycin sensitive aminopeptidase, NPEPPS, as a novel hit. Depletion of NPEPPS resulted in sensitizing resistant bladder cancer cells to cisplatin in vitro and in xenograft experiments. Pharmacologic inhibition of NPEPPS with tosedostat in cells and in chemoresistant, bladder cancer patient-derived tumoroids improved response to cisplatin. Prior work found NPEPPS in a protein complex with volume regulated anion channels (VRACs) in several cell line models. Interestingly, depletion of two VRAC subunits, LRRC8A and LRRC8D, known importers of intracellular cisplatin, enhanced resistance to cisplatin. Our findings support NPEPPS as a novel and druggable driver of cisplatin resistance with the potential for rapid translation to clinical investigation.

2024-02-20 | PXD024742 | Pride

Dynamic response of annexin A11-associated gene expression to cisplatin treatment

2009-12-01 | GSE13893 | GEO

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