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Human A375 melanoma cell line treated with ciclopirox and crizotinib

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE59340 | GEO | 2018/01/01

SECONDARY ACCESSION(S): PRJNA255119

REPOSITORIES: GEO

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Human WM35 melanoma cell line treated with ciclopirox and crizotinib

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

Human A375 melanoma cell line treated with trifluorothymidine (TFT) and lactimidomycin (LTM)

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 trifluridine or lactimidomycin at 75% inhibitory concentrations (IC75, determined previously at 72h of treatment) or DMSO (vehicle) for 8h or 24h before harvest.

2018-01-01 | GSE59183 | GEO

Human WM35 melanoma cell line treated with trifluorothymidine(TFT) and lactimidomycin(LTM)

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 trifluridine or lactimidomycin at 75% inhibitory concentrations (IC75, determined previously at 72h of treatment) or DMSO (vehicle) for 8h or 24h before harvest.

2018-01-01 | GSE59341 | GEO

Crizotinib v. DMSO in SW480 cells

Project description:SW480 cells were treated with 2uM crizotinib for 72h (versus DMSO)

2017-04-25 | GSE93124 | GEO

Profile of mRNA transcriptomes of E. coli affected by antifungal agent ciclopirox

Project description:Purpose: The identification of genes and regulatory pathways involved in the susceptibility to ciclopirox activity Methods: mRNA profiles of ciclopirox treatment in wild-type strain using Illumina sequencing. Results: Using an optimized data analysis workflow, we mapped about 1 million sequence reads per sample to the E. coli K-12 genome and identified 4,290 transcripts in wild-type with our without sublethal concentration of ciclopirox (12.5 ug/mL). Overall, this is the first genome-wide level analysis of ciclopirox as an antibacterial against Gram-negative bacteria and shown that >13 pathways were affected by ciclopirox with the change of expression level of >10 genes. Data analysis with CLRNASeq showed some differently expressed transcripts by ciclopirox treatment. Conclusions: Our study represents the first detailed analysis of ciclopirox-affected transcriptomes, with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. Our results show that NGS offers a comprehensive and more accurate quantitative and qualitative evaluation of mRNA content within a cell or tissue. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions.

2020-02-05 | GSE110854 | GEO

Microarray gene expression analysis of human melanoma A375 cells treated with 0.5mM phenformin against untreated control

Project description:The aim of this study was to characterize the effect of phenformin on human melanoma cells at the transcritpional level. Experimentally, A375 cells have been treated or untreated with 0.5mM phenformin for 72h, then lysed for RNA isolation.

2018-11-01 | E-MTAB-6665 | biostudies-arrayexpress

Targeting Myc signaling pathway by inhibition of histone demethylase JMJD2B (ciclopirox)

Project description:Epigenetic alterations appear to modulate Myc signaling. We investigated the role of the histone demethylase JMJD2B in Myc-mediated neuroblastoma pathogenesis. We demonstrate that Myc physically interacts with and recruits this epigenetic modifier, which removes repressive H3K9 methyl marks from Myc-target genes. JMJD2B regulates neuroblastoma proliferation and, together with MYCN amplification, identifies a subgroup of poor prognosis patients. We identify a novel histone demethylase inhibitor, ciclopirox, which targets JMJD2B and, consequently, Myc signaling, thereby inhibiting neuroblastoma proliferation and inducing differentiation. In xenograft studies, genetic and pharmacologic inhibition of JMJD2B resulted in significant tumor growth restriction. Our findings provide insight into epigenetic regulation of Myc via histone methylation and proof-of-concept for pharmacologic inhibition of histone demethylases to target Myc signaling in cancer. 8 samples were treated with vehicle or ciclopirox.

2014-01-01 | E-GEOD-45969 | biostudies-arrayexpress

Gene expression profiles of an ALK-fusion driven cell line and its derivatives resistant to crizotinib alone or resistant to crizotinib plus afatinib

Project description:Despite the initial benefit of the tyrosine kinase inhibitors targeting ALK gene fusions in non-small cell lung cancer, resistance to ALK inhibitors is almost inevitable. To determine the acquired resistance mechanism to ALK inhibition, we generated crizotinib-resistant ALK lines by chronically treating H3122 cells (driven by EML4-ALK) with an ALK inhibitor, crizotinib for approximately 3 months. RNA-seq and differential expression analyses were performed to determine the transcriptional changes of H3122-CR cells in comparison to parental H3122 cells. Because we demonstrated EGFR could mediate the early adaptive resistance to crizotinib, we further explored the mechanism that contributes to the resistance to the combination of crizotinib and afatinib. H3122-CAR (crizotinib and afatinib-resistant) cells were generated by treating them with a combination of crizotinib and afatinib for approximately 6 months and then profiled by RNA-seq to determine the associated transcriptional reprogramming.

2023-07-31 | GSE239666 | GEO

The effect of crizotinib in A549 lung cancer cell

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

Fasting potentiates the anticancer activity of Crizotinib

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

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