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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Dual inactivation of Akt and ERK by small molecule TIC10 signals Foxo3a nuclear translocation, TRAIL gene induction and potent anti-tumor effects

ABSTRACT: TIC10-induced transcriptional changes at 48hrs in HCT116 p53-null cells (10uM). Six samples of HCT116 p53-null cells with TIC10 (10uM) or DMSO treatment. Three replicates each.

ORGANISM(S): Homo sapiens

SUBMITTER: Joshua Allen

PROVIDER: E-GEOD-34194 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Dual inactivation of Akt and ERK by TIC10 signals Foxo3a nuclear translocation, TRAIL gene induction, and potent antitumor effects.

Allen Joshua E JE Krigsfeld Gabriel G Mayes Patrick A PA Patel Luv L Dicker David T DT Patel Akshal S AS Dolloff Nathan G NG Messaris Evangelos E Scata Kimberly A KA Wang Wenge W Zhou Jun-Ying JY Wu Gen Sheng GS El-Deiry Wafik S WS

Science translational medicine 20130201 171

Recombinant tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is an antitumor protein that is in clinical trials as a potential anticancer therapy but suffers from drug properties that may limit efficacy such as short serum half-life, stability, cost, and biodistribution, particularly with respect to the brain. To overcome such limitations, we identified TRAIL-inducing compound 10 (TIC10), a potent, orally active, and stable small molecule that transcriptionally induces TRAIL in a ...[more]

PMID: 23390247

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Dual inactivation of Akt and ERK by small molecule TIC10 signals Foxo3a nuclear translocation, TRAIL gene induction and potent anti-tumor effects

Project description:TIC10-induced transcriptional changes at 48hrs in HCT116 p53-null cells (10uM).

2013-03-08 | GSE34194 | GEO

Anti-cancer agent ONC201 activates early ATF4/DR5 upregulation, and cell death associated with XIAP inhibition

2016-06-01 | GSE72865 | GEO

Anti-cancer agent ONC201 activates early ATF4/DR5 upregulation, and cell death associated with XIAP inhibition

Project description:Two experiments were performed with ONC201/TIC10 in human colon cancer cell lines. The first experiment is TIC10-induced transcriptional changes at 48hrs in HCT116 p53-null cells (10uM). The second experiment is RKO cells, with and without acquired resistance to ONC201, treated with with ONC201 (10uM) for 48 hrs. For the first experiment, six samples of HCT116 p53-null cells with TIC10 (10uM) or DMSO treatment. Three replicates each. For the second experiment, six samples of wild-type RKO cells with ONC201 (10uM) or DMSO treatment and the same treatments for RKO cells with acquired resistance to ONC201.

2016-06-01 | E-GEOD-72865 | biostudies-arrayexpress

Mutant p53 cancers reprogram macrophages to tumor supporting macrophages via exosomal miR-1246

Project description:exosomes isolated from: HT29+control shRNA; HT29+p53 shRNA; HCT116 WT p53; HCT116 mutant p53; HCT116 null p53; media used as negative control

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Dual inactivation of Akt and ERK by TIC10 signals Foxo3a nuclear translocation, TRAIL gene induction, and potent antitumor effects.

Project description: Not available

| S-EPMC4535715 | biostudies-literature

Gene expression profiling of CYC116 and ZM447439 resistant HCT116 wild type and HCT116 p53 null clones in comparison to parent cell lines

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].

2012-04-01 | E-MEXP-3526 | biostudies-arrayexpress

The DNA binding selectivity by wild-type p53 and PANDAs

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.

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Identification of p53-regulated genes in wild-type p53 or p53-null HCT116 cells

Project description:Identification of p53-regulated genes in wild-type p53 or p53-null HCT116 cells

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Transcription profiling by array of human colorectal cancer epithelial (HCT116) p53 null cells treated with SN38 for 6, 12 and 24h

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.

2007-11-30 | E-MEXP-1194 | biostudies-arrayexpress

Role of SMAR1 in global gene regulation through interaction with tumor suppressor p53

Project description:Scaffold Matrix Attachment Region binding protein 1, SMAR1 has vital role to play as a general repressor of transcription. SMAR1 is known to retard cell cycle progression and delay tumor growth in mice. Further, it forms a ternary complex with p53-Mdm2 and inhibit p53-mediated transcription. Thus, SMAR1 can potentially alter p53 function and orchestrate different set of genes in p53-dependent and p53-independent manner. The present study aims to decipher the potential role of SMAR1 in global transcription regulation and to study role of p53 in the process. Towards this objective, chromatin immunoprecipitation combined Next-generation sequencing (ChIP-Seq) was performed using HCT116 and HCT116 p53-/- cell samples. The α-SMAR1 antibody was used for such ChIP experiments which was already tested by Wastern blot assays and found to be SMAR1 specific. The sequence data generated was then analyzed and the results obtained are (1) Higher genomic occupancy of SMAR1 in HCT116 (wild type) than HCT116 p53-/- (P53 null) data set (2) For peaks within ±5kb of TSS, SMAR1 had the highest predisposition to bind upstream of the TSS in close proximity, i.e., -1 to 0 kb that represents the promoter region of the gene (3) SMAR1 was found to target 5617 genes (unique in Wild type) , 8198 genes (unique in Null) and 1876 genes that were common in both the samples (4) In silico motif search indicated that SMAR1 binds to a dinucleotide T(C/G) repeat sequence (5) Functional Annotation of targets revealed that the predicted target genes are involved in apoptosis, epigenetics, cell cycle, cell signalling, neuronal genes, transcription, metabolism etc. The target also include noncoding RNAs genes such as microRNAs /lincRNAs.

2016-10-13 | GSE70058 | GEO

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