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: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: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.
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:microRNA expression profiles show altered patterns in cell lines with acquired resistance to the BRAF inhibitor compared to the parental cell lines, and common miRNAs regulated in the resistant variants
Project description:Malignant rhadboid tumours (MRTs) are lethal paediatric cancers characterised by a deficiency in the SWI/SNF subunit SMARCB1. Here we employ an integrated molecular profiling and chemical biology approach to demonstrate that the receptor tyrosine kinases (RTKs) PDGFRα and FGFR1 are coactivated in MRT cells and that dual blockade of these receptors has synergistic efficacy. Gene expression analysis of the four cell lines in the presence of TKI showed that the resistant sublines clustered together with the untreated parental cells and confirmed that PDGFRA was among the most highly downregulated genes in the resistant cells.
Project description:Copy number profiling of MKN45T 5-FU resistant gastric cancer cell lines and its parental cell line MKN45. We hypothesized that a detailed fine-scale survey of genomic CNAs might reveal the mechanism for acquired resistant to 5-FU in gastric cancer.