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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

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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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Crotonylomics sequencing of human colon cancer cell lines

Project description:P53 mutation is closely associated with the occurrence and progression of colon cancer. In this project, we did crotonylomics sequencing by using human colon cancer homologous cell line pair-HCT116+/+(with wild type p53) and HCT116-/- (with null p53). Crotonylomics sequencing results showed that p53 deficiency regulated crotonylation of non-histone proteins.

2024-05-22 | PXD047258 | Pride

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

Project description: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 p53-independent manner and crosses the blood-brain barrier. TIC10 induces a sustained up-regulation of TRAIL in tumors and normal cells that may contribute to the demonstrable antitumor activity of TIC10. TIC10 inactivates kinases Akt and extracellular signal-regulated kinase (ERK), leading to the translocation of Foxo3a into the nucleus, where it binds to the TRAIL promoter to up-regulate gene transcription. TIC10 is an efficacious antitumor therapeutic agent that acts on tumor cells and their microenvironment to enhance the concentrations of the endogenous tumor suppressor TRAIL.

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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].

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The DNA binding selectivity 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

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