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GIST cell cycle dysregulation is required for progression to high-risk disease but not for resistance to kinase inhibitors

ABSTRACT: Background: To understand the transcriptional consequences of a TP53 modulation in the GIST cell context, we treated GIST430 with increasing doses of the MDM2-inhibitor nutlin-3 (racemate).

ORGANISM(S): Homo sapiens

PROVIDER: GSE59841 | GEO | 2014/12/25

SECONDARY ACCESSION(S): PRJNA256344

REPOSITORIES: GEO

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GIST cell cycle dysregulation is required for progression to high-risk disease but not for resistance to kinase inhibitors

Project description:Background: To understand the transcriptional consequences of a TP53 modulation in the GIST cell context, we treated GIST430 with increasing doses of the MDM2-inhibitor nutlin-3 (racemate). In this study, 3’ end RNA Sequencing (3SEQ) was used to expression profile GIST430 cell lines treated with DMSO and Nutlin-3, 2.5µM or 10µM for 18h. Then the gene expression profiles between these concentrations were compared.

2014-12-25 | E-GEOD-59841 | biostudies-arrayexpress

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Genome-wide CRISPR screen of MOLM13 cells after Idasanutlin treatment

Project description:Targeting MDM2 is an attractive therapeutic approach for TP53 wild-type (WT) tumors, including the majority of de novo acute myeloid leukemia (AML) cases. However, patients with WT TP53 have shown variable responses to MDM2 inhibitors in clinical trials, highlighting the need to identify additional biomarkers to maximize the chances of clinical success. We performed CRISPR-Cas9 knockout screens to identify genes that confer resistance to an MDM2 inhibitor idasanutlin. We did not find recurrent sgRNA hits or mutations in p53 downstream targets, such as CDKN1A, BAX, PMIAP1, and BBC3, apart from TP53. This was consistent with the results of individual knockout validation experiments and exome sequencing data from idasanutlin resistant cell lines generated form long-term exposure to low doses of idasanutlin. RNA-seq differential expression analysis revealed that major p53 downstream targets were upregulated in both idasanutlin-sensitive MOLM13 and resistant OCIAML3 cell lines after idasanutlin treatment. These findings highlight the pleiotropic functions of TP53 and suggest that the loss of individual downstream targets of TP53 does not significantly contribute to MDM2 inhibitor resistance.

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Genome wide analysis of mouse gastrointestinal stromal tumors (GIST) in a mouse model of spontaneous GIST.

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Project description:ETV1 is highly expressed in GIST cells and required for their survival and growth. To identify genes and pathways regulated by ETV1 in GIST, we performed expression profiles of GIST cells after ETV1 knockdown. Two GIST cell lines (GIST48 and GIST882) were infected in duplicate with three shRNA viruses (Scrambled, ETV1sh1-B11TRCN0000013923, ETV1sh2-TRCN0000013925). Four days after infection, RNA was harvested for expression profiling.

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