HSP90 inhibitor resistant cells
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00010002336 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Genetic analysis of K562 cell which are resistant against HSP90 inhibitors.
| EGAS00001006381 | EGA
Project description:Analysis of the acquired copy number profile in K562 cell which got resistant against HSP90 inhibitors.
| EGAS00001006385 | EGA
Project description:A comparison between parental K562 cells (CML) and two clones derived from this cell line : ImaR and PDR which are resistant against Imatinib mesylate and PD166326 respectively , two inhibitors of BCR-ABL. Keywords: gene expression, comparison
2009-06-01 | GSE10382 | GEO
Project description:Multidrug resistance (MDR) frequently develops in cancer patients exposed to chemotherapeutic agents and is usually brought about by over-expression of P-glycoprotein (P-gp) which acts as a drug efflux pump. MiRNAome profiling using next-generation sequencing identified differentially expressed microRNAs (miRs) between parental K562 cells and MDR K562 cells (K562/ADM) induced by chronic adriamycin treatment. MiRNAome profiling in untreated K562 cells and K562 cells exposed to long-term adriamycin treatment
2013-10-29 | E-GEOD-51774 | biostudies-arrayexpress
Project description:Genome variation profiling of lung adenocarcinoma cells comparing untreated NCI-H1975 cells with CNX-2006-resistant untreated cells. Goal was to determine the potential mechanism of resistance to mutant EGFR-TKIs and rationally design novel strategies for the treatment of EGFR-mutant lung cancer patients. Two-condition experiment: NCI-H1975 parental cells vs CNX-2006-resistant cells. Pooled DNA from healthy volunteers was used as reference.
2015-07-01 | E-GEOD-53234 | biostudies-arrayexpress
Project description:We applied DNA content flow cytometry to a series of prostate cancer (PC) patient derived tumor xenografts (PDTXs). We interrogated purified sorted tumor fractions from each sample with whole genome copy number variant (CNV) analyses. These identified a variety of somatic genomic lesions targeting genes and cellular pathways in PC. Of significant interest are lesions that may affect responses to therapies. Guided by the genomic alterations in these models and interrelated mechanisms between androgen signaling axis, the cell cycle, and AKT pathway, we identified and investigated the combination of CDK4/6 inhibitors with AKT inhibitors as a potential therapy for patients with mCRPC. Using 3-D spheroid drug assays followed by in vivo experiments in three unique PDTX models, these preclinical results highlight the potential use of CDK4/6 inhibitor with AKT inhibitors for the treatment of mCRPC who have intact retinoblastoma pathway, thereby, providing the experimental data support and rationale for future clinical investigation
2023-05-31 | GSE230411 | GEO
Project description:Wnt/β-catenin signaling is activated in colorectal cancer (CRC) and is involved in CRC growth. Tankyrase, a poly(ADP-ribose) polymerase family member, destabilizes Axin and positively regulates the Wnt/β-catenin signaling. Tankyrase inhibitors efficiently suppress CRC cell proliferation. We established 320-IWR cells, which showed resistance to tankyrase inhibitor IWR-1, from human CRC COLO-320DM cells. We analyzed gene expression profile of 320-IWR cells (320IWR_1,_2) and parental COLO-320DM cells (COLO320_1,_2).
2016-11-01 | GSE86061 | GEO
Project description:Metabolic reprogramming, due in part to the overexpression of metabolic enzymes, is a key hallmark of cancer cells. Lactate dehydrogenase (LDHA), a metabolic enzyme that catalyzes the interconversion of lactate and pyruvate, is overexpressed in a wide variety of cancer types, including pancreatic ductal adenocarcinoma (PDAC). Furthermore, the genetic or pharmacological inhibition of LDHA suppresses cancer growth, demonstrating a cancer-promoting role for this enzyme. Therefore, several pharmacological LDHA inhibitors are being developed and tested as potential anti-cancer therapeutic agents. Because cancer cells are known to rapidly adapt and become resistant to anti-cancer therapies, in this study, we modeled the adaptation of cancer cells to LDHA inhibition. Using PDAC as a model system, we studied the molecular aspects of cells resistant to the competitive LDHA inhibitor sodium oxamate. We performed unbiased RNA-sequencing (RNA-seq), assay for transposase-accessible chromatin with sequencing (ATAC-seq), and metabolomics analyses of parental and oxamate-resistant PDAC cells treated with and without oxamate to identify the transcriptional, chromatin, and metabolic landscapes of these cells. We found that oxamate-resistant PDAC cells were significantly different from parental cells at the levels of mRNA expression, chromatin accessibility, and metabolites. Additionally, an integrative analysis combining the RNA-seq and ATAC-seq datasets identified a subset of differentially expressed mRNAs that directly correlated with changes in chromatin accessibility. Finally, functional analysis of differentially expressed metabolic genes in parental and oxamate-resistant PDAC cells treated with and without oxamate, together with an integrative analysis of RNA-seq and metabolomics data, revealed changes in metabolic enzymes that might explain the changes in metabolite levels observed in these cells. Collectively, these studies identify the transcriptional, chromatin, and metabolic landscapes of LDHA inhibitor resistance in PDAC cells. Future functional studies related to these changes remain necessary to reveal the direct roles played by these changes in the development of LDHA inhibitor resistance and uncover approaches for more effective use of LDHA inhibitors in cancer therapy.
2022-08-02 | GSE164976 | GEO
Project description:Metabolic reprogramming, due in part to the overexpression of metabolic enzymes, is a key hallmark of cancer cells. Lactate dehydrogenase (LDHA), a metabolic enzyme that catalyzes the interconversion of lactate and pyruvate, is overexpressed in a wide variety of cancer types, including pancreatic ductal adenocarcinoma (PDAC). Furthermore, the genetic or pharmacological inhibition of LDHA suppresses cancer growth, demonstrating a cancer-promoting role for this enzyme. Therefore, several pharmacological LDHA inhibitors are being developed and tested as potential anti-cancer therapeutic agents. Because cancer cells are known to rapidly adapt and become resistant to anti-cancer therapies, in this study, we modeled the adaptation of cancer cells to LDHA inhibition. Using PDAC as a model system, we studied the molecular aspects of cells resistant to the competitive LDHA inhibitor sodium oxamate. We performed unbiased RNA-sequencing (RNA-seq), assay for transposase-accessible chromatin with sequencing (ATAC-seq), and metabolomics analyses of parental and oxamate-resistant PDAC cells treated with and without oxamate to identify the transcriptional, chromatin, and metabolic landscapes of these cells. We found that oxamate-resistant PDAC cells were significantly different from parental cells at the levels of mRNA expression, chromatin accessibility, and metabolites. Additionally, an integrative analysis combining the RNA-seq and ATAC-seq datasets identified a subset of differentially expressed mRNAs that directly correlated with changes in chromatin accessibility. Finally, functional analysis of differentially expressed metabolic genes in parental and oxamate-resistant PDAC cells treated with and without oxamate, together with an integrative analysis of RNA-seq and metabolomics data, revealed changes in metabolic enzymes that might explain the changes in metabolite levels observed in these cells. Collectively, these studies identify the transcriptional, chromatin, and metabolic landscapes of LDHA inhibitor resistance in PDAC cells. Future functional studies related to these changes remain necessary to reveal the direct roles played by these changes in the development of LDHA inhibitor resistance and uncover approaches for more effective use of LDHA inhibitors in cancer therapy.
2022-08-02 | GSE164974 | GEO
Project description:Transcriptional profiling of human lung adenocarcinoma cells comparing control untreated SPC-A1 cells with SPC-A1 cells treated with 300 µg/ml mAb NJ001 for 36h
2014-08-01 | GSE59655 | GEO