Expression data from ASPC1-GFP PDAC cells treated with fluvastatin
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE161536 | GEO | 2021/11/23
REPOSITORIES: GEO
Similar Datasets
Project description:Expression data from ASPC1-GFP PDAC cells treated with fluvastatin
| PRJNA678661 | ENA
Project description:Cisplatin is a broad-spectrum anticancer drug, which is estimated to be administered to 40-80% of patients undergoing chemotherapy. However, its clinical utility is often limited due to factors that include acquired resistance of cancer cells to cisplatin. Because cisplatin is currently evaluated as a prospective agent for combined chemotherapy of pancreatic ductal adenocarcinoma (PDAC), we have investigated mechanisms involved in the acquired resistance of PDAC cells to cisplatin using gene expression study of two different parental-resistant pairs of PDAC cell lines. We have developed cisplatin-resistant cell lines AsPC1-R and BxPC3-R from their parental PDAC cell lines AsPC1 and BxPC3, respectively, by culturing them in medium with step-wise increasing concentration of cisplatin. Parental and resistant pairs of PDAC cells were analyzed by whole-transcript gene expression analysis.
2015-11-30 | GSE73978 | GEO
Project description:Transcriptional profiling comparing human AsPC1 PDA cells transduced with either CFP control or myristoylated-AKT orthotopically grown in pancreata of lean vs obese Rag1-/- immunodeficient mice for 5 weeks (100,000 cells/pancreas). The Goal was to determine the transcriptional deregulation of Obesity-driven and AKT-driven tumors.
2017-05-26 | GSE99289 | GEO
Project description:Fluvastatin has been identified as novel inhibitors of metastasis in pancreatic cancer. In multiple in vivo and in vitro experiments the compounds phenotypic effects was validated. Since under drug treatment the transcriptomic changes in examined cell lines were rather small, we expected the underlying mechanistic effect to be on the level of the proteome and more importantly the phospho-proteome. To evaluate this assumption we performed label-free full proteome and phosphoproteomics experiments on Fluvastatin treated ASPC1 cells.
2021-11-29 | PXD022345 | Pride
Project description:Background: Cholesterol pathway inhibition by statins prevents breast cancer development in mouse models of breast cancer but their efficacy is not very high (about 50%) . Therefore, the goal of this study is to investigate if the fluvastatin mediated upregulation in the steroid biosynthesis pathway genes limit the efficacy of statin chemoprevention. Methods: A published gene signature of statin resistance was validated in cell line-based models of inherent and acquired resistance during breast cancer. These signatures were next validated in a mouse model of hormone receptor negative breast cancer. Results: We found more than 70% of a published multi-gene fluvastatin resistance signature to be significantly upregulated in an inherently resistant cell line relative to fluvastatin sensitive cell line. We found this inherent statin resistance gene signature to be also shared with the signature of acquired resistance to fluvastatin (13 / 23 total genes). These 13 inherent resistance genes and 10 additional genes mapped to 2 of the top 3 deregulated pathways that are steroid-, and terpenoid backbone- biosynthesis pathway. Next, we tested if one or multiple genes of statin resistance signature, could predict efficacy of statin chemoprevention in the SV40 C3TAg transgenic mouse model. We found upregulation of a large number (19/24) of genes in the tumor bearing mammary glands, suggesting that upregulation of these pathways drives resistance to statin chemoprevention. A subset of 13-genes from this panel was significantly associated with response to statin treatment, as was the expression level of HMGCR alone in a mouse model of breast cancer. Lastly, we studied if a 10-day period of fluvastatin treatment to SV40C3 TAg mice, can also trigger the upregulation of these genes and provide an early signal of statin resistance. These experiments showed that a 10-day period is insufficient to cause a feedback upregulation in steroid biosynthesis pathway genes and thus cannot be used as an early biomarker to detect resistance to fluvastatin. Conclusions: High basal or restorative upregulation in the steroid biosynthesis pathway gene expression after fluvastatin treatment appears to be strongly associated with resistance to statin chemoprevention for breast cancer and may serve as a biomarker to identify patients that are most likely to respond to statins or develop resistance.
2022-03-01 | GSE174673 | GEO
Project description:Genome-wide studies on pancreatic adenocarcinoma (PDAC) have indicated that numerous genes involved in carcinogenesis are highly methylated in their promoter regions but nevertheless strongly transcribed. It has been proposed that transcription factors may specifically bind to methylated promoters and up-regulate transcription. Screening a protein microarray presenting 658 transcription factors, we found that molecules of the NFAT (Nuclear Factor of Activated T-Cells) family preferentially bound to methylated promoter sequences. One family member – NFATc1 – was also strongly expressed in PDAC compared to control samples. To further identify targets of NFATc1 and study involved pathways, we have used siRNA to knockdown NFATc1 in three pancreatic cancer cell lines (Panc1, MiaPaCa2, AsPC1) with the help of the illumina beadchip arrays and we compared the transcriptional profiles of the cell lines under different knockdown conditions. We identify ALDH1A3 as direct targets of NFATc1, that NFATc1 binds the methylated promoter of ALDH1A3 and accelerate PDAC progression.
2021-11-05 | E-MTAB-10122 | biostudies-arrayexpress
Project description:Clinical data of patients suffering from COVID-19 have indicated that statin therapy, used to treat hypercholesterolemia, is associated with a better clinical outcome. We therefore investigated the effect of statins on SARS-CoV-2 infection in human lung cells and found that fluvastatin inhibited coronavirus infection, while other tested statins did not. Fluvastatin inhibited high and low pathogenic coronaviruses in vitro and ex vivo in a dose-dependent manner. Proteomic analyses of infected versus uninfected lung epithelial cells treated with fluvastatin, simvastatin, or rosuvastatin revealed that all tested statins modulated the cholesterol synthesis pathways without compromising the innate antiviral immune response. Strikingly, fluvastatin treatment uniquely affected the proteome of SARS CoV 2 infected cells, specifically downregulating proteins that modulate protein translation and viral replication. These results suggest that statin therapy poses no additional risk to individuals exposed to SARS-CoV-2 and that fluvastatin may have a moderate beneficial effect on SARS CoV-2 infection by modulating protein translation.
2021-12-07 | PXD023422 | Pride
Project description:The present gene expression array study of fluvastatin effects on monocytes from SLE patients show that fluvastatin has a global anti-inflammatory effect on monocytes, which includes attenuated expression of several proinflammatory cytokines, and regulated expression of molecules mediating lipoprotein signaling and cholesterol metabolism, as well as atherosclerosis and inflammatory signaling.
2014-03-12 | GSE45422 | GEO
Project description:The CREB binding protein inhibitor ICG-001 suppresses pancreatic cancer growth We used microarrays to detail global gene expression changes in the pancreatic cancer cell line AsPC1 following treatment with ICG-001 or siRNA-mediated knockdown of CTNNB1 (beta-catenin) AsPC1 cells were treated with 10uM ICG-001 or vehicle control (DMSO) for either 6 hours or 24 hours. AsPC-1 cells were also separately transfected with 20nM control siRNA or CTNNB1 siRNA for 48 hours. RNA was extracted at these time points for hybridization to Affymetrix microarrays
2014-07-15 | E-GEOD-57728 | biostudies-arrayexpress
Project description:Despite advances in melanoma treatment, more than 70% of patients with distant metastasis die within 5 years. Proactive treatment of early melanoma to prevent metastasis could save lives and reduce overall healthcare costs. Currently, there are no treatments specifically designed to prevent early melanoma from progressing to metastasis. We used the Connectivity Map (cMap) to conduct an in silico drug screen and identified HMGCR inhibitors (statins) as a drug class that might prevent melanoma metastasis. To confirm the in vitro effect of statins, RNA-sequencing was completed on A375 cells after treatment with fluvastatin to describe changes in the melanoma transcriptome. Statins induced differential expression in genes associated with metastasis and used in commercially available prognostic tests for melanoma metastasis.
2023-11-04 | GSE160870 | GEO