Crizotinib v. DMSO in SW480 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE93124 | GEO | 2017/04/25
SECONDARY ACCESSION(S): PRJNA361139
REPOSITORIES: GEO
Similar Datasets
Project description:To generate drug signatures in human A375 melanoma cell lines. A375 cell line was plated at 4 x 105 cells/mL overnight and treated with ciclopirox or crizotinib at 75% inhibitory concentrations (IC75, determined previously at 72h of treatment) or DMSO (vehicle) for 8h or 24h before harvest.
2018-01-01 | GSE59340 | GEO
Project description:To generate drug signatures in human WM35 melanoma cell line. WM35 cell line was plated at 4 x 105 cells/mL overnight and treated with ciclopirox or crizotinib at 75% inhibitory concentrations (IC75, determined previously at 72h of treatment) or DMSO (vehicle) for 8h or 24h before harvest.
2018-01-01 | GSE59342 | GEO
Project description:This experiment is designed to detect genes differentially expressed in 2uM erlotinib treatment versus DMSO treatment and to identify differential gene set enrichments.
2015-03-19 | GSE67051 | GEO
Project description:We used a CRISPR-Cas9-based genome-wide guide RNA (sgRNA) library to identify genes responsible for driving drug resistance in ALK+ ALCL cells under crizotinib treatment.We screened 4 diffrerent ALK+ ALCL cell lines, TS, SU-DHL1, COST and KARPAS299. Every cell line was transduced with GeCKO A and GeCKO B sgRNA libraries separately. After puromycin selection, cells were splitted into 3 groups: Day 0 (baseline time point), crizotinib treated group (treated for 14 days) and DMSO treated group (treated for 14 days). TS and SU-DHL1 cells were treated with 40nM criztonib for 14 days and at the end of this period crizotinib concentration was increased to 80nM. COST cells received 50nM crizotinib for 14 days. KARPAS299 cells first received 50nM crizotinib for 14 days and at the end of this period crizotinib concentration was increased to 100nM. Crizotinib concentrations were determined based on their sensitivity for crizotinib for each cell line. The screening was repeated twice for TS and SU-DHL1 ALK+ ALCL cells. DNA isolotation was performed from all groups and each sgRNA sequence served as a barcode for Next Generation Illumina-based DNA sequencing. We compared enriched sgRNA sequences between Day 0 and DMSO conditions. We found that while PTPN2 was a top hit for all 4 ALK+ ALCL cells, PTPN1 was a top hit for TS and SU-DHL1 cells. We subsequently validated roles of PTPN1 and PTPN2 in crizotinib resistance separately. We demonstrated that both PTPN1 and PTPN2 can drive crizotinib resistance in ALK+ ALCL cells. In this study, we found two phosphatases, PTPN1 and PTPN2, involved in drug resitance in ALK+ ALCL using a CRSIPR Cas9-based screening approach. These two phosphatases regulate ALK phospharylation and therefore affect downstream signalling pathways involved in tumor growth and proliferation.
2023-03-15 | GSE152926 | GEO
Project description:TGFb and/or crizotinib were treated on A549 cell line to understand molecular mechanisms of action of crizotinib in TGF signaling pathway in lung cancer through gene expression profile data.
2022-09-27 | GSE189047 | GEO
Project description:SW480 were stably transfected with an episomal plasmid expressing GFP and miRNA34 from a bidirectional doxycyclin regulatable promoter (Bornkamm et al Nucleic Acids Res. 2005 Sep 7;33(16)). Polyclonal cell lines were obtained by selection with Hygromycin at 350ug/ml for 10 days. The cell llnes identified as GFP only express GFP, whereas the cell lines identified as miRNA34a express both GFP and miRNA34 under doxycyclin control. For the present experiment, cells were treated with 1ug/ml Docycyclin for 72h. Cells were harvested and total RNA was isolated using Trizol (Invitrogen). After RNA cleanup (RNeasy, Qiagen) Affymetrix 133 Plus 2.0 micorarrays were hybridized using standard techniques. Keywords: Cell line transfection
2007-08-20 | GSE7678 | GEO
Project description:In tumor cells, stepwise oncogenic deregulation of signaling cascades induces alterations of cellular morphology and promotes the acquisition of malignant traits. Using a panel of small molecular inhibitors, we established associated gene expression signatures of key signaling hubs. SW480 cells were grown in DMEM, 10% FCS, and treated for 24h with the following inhibitors or with solvent (DMSO): SU5402 (42uM); U0126 (10uM), SP600125 (20uM), LY294002 (20uM)
2011-06-03 | E-GEOD-29689 | biostudies-arrayexpress
Project description:Background: Tyrosine kinase inhibitors (TKIs) are widely used for treating solid and hematologic malignancies. However, their efficacy is frequently short lived, warranting the search for safe potentiation strategies. Short courses of fasting were shown to sensitize cancer cells to chemo- and radiotherapy while increasing the resistance of healthy tissues to the same agents. The purpose of this study was to assess the potential of fasting to increase the efficacy of TKIs. Methods: starvation-mimicking culture conditions were studied for their ability to potentiate the effects of Epidermal Growth Factor Receptor (EGFR), Human Epidermal Growth Factor Receptor 2 (HER2), Anaplastic Lymphoma Kinase (ALK) and multitarget TKIs in terms of cancer cell growth, signaling cascades inhibition, and changes in gene expression profile in TKI-sensitive cancer cells. In vivo, the activity of crizotinib or regorafenib, weekly cycles of fasting, or their combination was compared in tumor xenografts models. Results: In vitro, starvation-mimicking culture conditions increased the ability of TKIs to block cancer cell growth and to inhibit the mitogen-activated protein kinase (MAPK) signaling pathway. At the gene expression profile level, starvation and crizotinib led to similar changes, but their combination strengthened Rb-, MYC-, and E2F-dependent transcription inhibition. In vivo, both TKIs and cycles of fasting slowed tumor growth, but, when combined, they were significantly more effective than either type of treatment alone. Conclusions: Cycles of fasting or of specifically designed fasting-mimicking diets should be evaluated in clinical studies as a means to potentiate the activity of TKIs in clinical use. RNA was collected from H3122 cells in 4 different conditions: serum, starvation, treated with Crizotinib, starvation and treated with Crizotinib. Each condition was run in quadruplicate
2016-07-03 | E-GEOD-62663 | biostudies-arrayexpress
Project description:The transcriptional profile of A673 parental and SP-2509 Drug resistant cells treated with DMSO and SP-2509 (2uM 48hrs)
2018-12-26 | GSE118864 | GEO