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Global analysis of p53-regulated transcription reveals its direct targets and unexpected regulatory mechanisms (GRO-Seq)

ABSTRACT: GRO-seq of HCT116 cells treated with Nutlin to activate p53

ORGANISM(S): Homo sapiens

PROVIDER: GSE53964 | GEO | 2014/05/15

SECONDARY ACCESSION(S): PRJNA234051

REPOSITORIES: GEO

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Global analysis of p53-regulated transcription reveals its direct targets and unexpected regulatory mechanisms (GRO-Seq)

Project description:GRO-seq of HCT116 cells treated with Nutlin to activate p53 HCT116 cells were treated with Nutlin or DMSO for 1 hour

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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Project description:Activation of p53 by the small molecule Nutlin can result in a combination of cell cycle arrest and apoptosis. The relative strength of these events is difficult to predict, leaving uncertainty as to the therapeutic benefits of Nutlin. Here, we report a new translation control mechanism shaping p53-dependent apoptosis. We performed polysomal profiling in the cell lines SJSA1 and HCT116, of which only the first undergoes robust cell death in response to p53 activation by Nutlin. We establish Nutlin-induced apoptosis in SJSA1 cells to be associated with a set of translationally enhanced mRNAs carrying a newly identified 3’UTR motif which we labeled CG-motif. We identified PCBP2 and DHX30 as interactor proteins of the CG-motif that are more abundant in HCT116 cells compared to SJSA1. The binding of DHX30 to the CG-motif detected in HCT116 cells was shown to be dependent on PCBP2. Interestingly, DHX30 depletion enhances polysome association of CG-motif mRNAs in HCT116 cells, shifting their outcome towards apoptosis. In U2OS, an osteosarcoma-derived cell line that unlike SJSA1 undergoes persistent cell cycle arrest in response to Nutlin, DHX30 is highly expressed and its depletion enhances the expression of CG-motif mRNAs.

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Project description:Identification of the RFX7-regulated transcriptome in Nutlin-3a and DMSO control treated HCT116 cells

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