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Expression analysis of Human pancreatic cancer cell line Panc1 pretreated with DMSO and Clofibrate.

ABSTRACT: Investigation of whole genome gene expression level changes of Panc1 pretreated with Clofibrate, compared to Panc1 pretreated with DMSO.

ORGANISM(S): Homo sapiens

PROVIDER: GSE69650 | GEO | 2015/06/09

SECONDARY ACCESSION(S): PRJNA286102

REPOSITORIES: GEO

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Expression analysis of Human pancreatic cancer cell line Panc1 pretreated with DMSO and Clofibrate.

Project description:Investigation of whole genome gene expression level changes of Panc1 pretreated with Clofibrate, compared to Panc1 pretreated with DMSO. Compare differentially expressed genes by analyzing mRNA profilings between DMSO and Clofibrate pretreating Panc1 cell.

2015-06-09 | E-GEOD-69650 | biostudies-arrayexpress

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Rat liver response to Clofibrate, DEHP or VPA

Project description:The project had 2 goals: 1) To evaluate the transcriptional response of 3 prototypical toxicants (Clofibrate, VPA, and DEHP) on rat lever. 2) To evaluate the impact pooling samples has on data analysis. Keywords = Clofibrate Keywords = Diethylhexyl phthalate Keywords = Phthalic acid bis(2-ethylhexyl ester) Keywords = Sodium Valproate Keywords = Valproic Acid Keywords = VPA Keywords = vehicle Keywords: other

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Profiling the Panc1 pancreatic cancer cell line following Gemcitabine treatment using single cell RNA sequencing

Project description:Pancreatic ductal adenocarcinoma (PDAC) often presents at late clinical stages, and most patients are managed solely through palliative chemotherapy. With no approved treatment modalities for patients who progress on broad-spectrum chemotherapy, we set to identify druggable targets to prevent or reverse resistance to the first line anti-neoplastic Gemcitabine. In our first experiment, we used the well-established Panc1 cell line as an in vitro model of PDAC. Panc1 cells were incubated with a tolerable dose of Gemcitabine in vitro, and examined alterations in gene expression via single cell RNA sequencing. In our subsequent studies, we incubated Panc1 cells with increasing doses of Gemcitabine for several passages, until viable in approximately 10x the known IC50 value. These cells were designated Panc1-GR. Based on our observations in the prior experiment, Panc1-GR cells were compared to those treated with wither the Calmodulin inhibitor W-7, Calcium chelator BAPTA-AM, or the calcium channel blocker Amlodipine. Through these efforts, we hope to better understand the mechanisms of Gemcitabine resistance in PDAC, as well as introduce new therapeutic strategies to reverse drug resistant phenotypes in the clinic.

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