Project description:Microarray-based gene expression analysis of HCT116 p53+/+ and HCT116 p53−/− treated with doxorubicin to activate p53 in time-dependent manner.
Project description:HCT116 and HCT116 p53 null were exposed to two Aurora kinase inhibitors (CYC116 and ZM447439) at cytotoxic concentrations. Within 4-5 weeks we were able to select and isolate 10 drug resistant clones from each group. 3 clones were selected for gene expression profiling using Affymetrix microarrays (Human Gene 1.0 ST Array). The samples in each group were initially given the code names as follows. Group 1. [R1.3, R4.2, R6.3: CYC116 p53 wild type], Group 2. [R8.7, R9.7, R10.7:CYC116 p53 null], Group 3. [R7.1, R15.1, R16.1:ZM447439 p53 wild type], and Group 4. [R1.5, R3.5, R4.5:ZM447439 p53 null). For publication purpose the names were later changed to, Group 1. [R1.1, R1.2, R1.3: CYC116 p53 wild type], Group 2. [R2.1, R2.2, R2.3:CYC116 p53 null], Group 3. [R3.1, R3.2, R3.3:ZM447439 p53 wild type], and Group 4. [R4.1, R4.2, R4.3:ZM447439 p53 null].
Project description:HCT116 p53 null cells were treated with 5nM SN38 (active metabolite of CPT-11) for 6, 12 and 24h. Following this RNA was harvested for transcriptional profiling.
Project description:We performed ChIP-seq analysis of p53-null HCT116 cells stably expressed wild-type p53 or mutant p53 followed by ATO treatment (PANDAs) to identify p53 binding characteristics by wild-type p53 and PANDAs.
Project description:We report the signaling pathway of Mina53 by depleting Mina53 in HCT116 p53+/+ cells and HCT116 p53-/- cells based on RNA-sequencing.