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Identification of a STAT2 transcriptome in HCT116 p53 null tumor xenografts

ABSTRACT: Identification of a STAT2 transcriptome in HCT116 p53 null tumor xenografts

PROVIDER: PRJNA564684 | ENA |

REPOSITORIES: ENA

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Identification of a STAT2 transcriptome in HCT116 p53 null tumor xenografts

Project description:Our previous study revealed that the transcription factor STAT2 promoted the growth of colorectal tumors, but the molecular mechanisms by which STAT2 contributes to tumor promotion are still unknown. Given that alterations in the tumor suppressor p53 gene are very common in colorectal cancer and critical in adenoma-carcinoma transition, we investigated whether STAT2 may also be implicated in disease progression when normal p53 function is disabled. We found Stat2 silencing in colon cancer cells deficient in p53 reduced the capacity of tumor cells to migrate and invade in vitro. We also determined that Stat2 silencing impaired tumor cells to metastasize to the liver. To begin to understand how STAT2 contributes to disease progression, we performed RNA-Seq analysis on colon tumor xenografts with the purpose to identify a STAT2 transcriptome. From this study, we identified a subset of STAT2 regulated genes that in future studies will confirm their role in colon carcinogenesis.

2020-11-17 | GSE137155 | GEO

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

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

| PRJNA517505 | ENA

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

Project description:Microarray-based gene expression analysis of HCT116 p53+/+ and HCT116 p53−/− treated with doxorubicin to activate p53 in time-dependent manner.

2019-01-29 | GSE125787 | GEO

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

2018-02-09 | MSV000082047 | MassIVE

RNAseq expression of p53-null and p53-null/PLK2-null mammary tumors

Project description:RNAseq expression of p53-null and p53-null/PLK2-null mammary tumors

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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

RNAseq expression of p53-null and p53-null/PLK2-null mammary tumors

Project description:Bulk tumor samples from p53-null and p53-null/ PLK2-null tumors that have been serially transplanted in Balb/c mice

2022-03-28 | GSE174683 | GEO

Expression profile of HCT116 p53+/+ and P53-/- cells treated with Leptomycin B

2010-07-31 | GSE17472 | GEO

Expression profile of HCT116 p53+/+ and P53-/- cells treated with Leptomycin B

Project description:HCT116 wild type cells express p53. The isogenic HCT116 p53KO cells have the p53 gene knocked out. Cells were treated for 16 hours. Dosages for leptomycin B treatment was 2 nM and 20 nM. Measuring the gene expression profile of the isogenic cell lines when the cells were treated with leptomycin B at different concentrations

2010-07-30 | E-GEOD-17472 | biostudies-arrayexpress

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