Project description:Parental and AqR cells were obtained at diferent time-points (Day1 and Day 18). Total RNA was extracted and submitted for RNA-seq. Differential expression was observed between parental and AqR cells. AqR cells were derived from parental cells by adding inhibitor (CAY10566) every 3 days until cells became resistant (at about 3 weeks).
Project description:Parental and AqR cells were obtained. DNA was purified and submited for sequencing. Differential chromatin accessiblity was observed. AqR cells were derived from parental cells by adding inhibitor (CAY10566) every 3 days until cells became resistant (at about 3 weeks).
Project description:RNA transcriptome sequencing analysis was performed in SNU-668 Erastin-resistant cells and SNU-668 parental cells, SNU-484 RSL3-resistant cells and SNU-484 parental cells
Project description:To determine the difference between MRTX849 parental and resistant cells in response to MRTX849 treatment, we used high-throughput next-generation sequencing technology to compare transcriptomics between parental and MRTX849-resistant MIA PaCa-2 cells that were cultured in the absence or presence of MRTX849 (1 uM, 4h).
Project description:To investigate the mechanism mediating resistance to CYH33 in ESCC cells, global gene expression was profiled with RNA-Seq in CYH33-resistant cells as well as their parental cells. Gene enrichment analysis revealed that RAS signaling pathway, PI3K-Akt signaling pathway and MAPK signaling pathway were highly activated in most CYH33-resistant cells. To analyze the difference of gene expression profiles between CYH33-resistant cells and their matched parental cells upon CYH33 treatment, cells were treated with CYH33 at 1 μM for 24 hours and RNA-seq was performed. Gene Set Enrichment Analysis was then carried out.
Project description:microRNA and mRNA profiling was conducted for parental cell lines and cell lines resistant to trifluridine in 3 colorectal cell lines (DLD-1, HCT-116, RKO). We hypothesized that a detailed comparison between miRNA and mRNA expression might reveal the mechanism for acquired resistant to trifluridine in colorectal cancer.
Project description:microRNA and mRNA profiling was conducted for parental cell lines and cell lines resistant to trifluridine in 3 colorectal cell lines (DLD-1, HCT-116, RKO). We hypothesized that a detailed comparison between miRNA and mRNA expression might reveal the mechanism for acquired resistant to trifluridine in colorectal cancer.