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Ribo_seq (aka ribosome profiling) analysis of control and Myc-induced U2OS cells

ABSTRACT: We used Ribo-seq to examine the effect of Myc activation on protein translation in U2OS cells and correalted these changes with alterations in RNA level measured by RNA-seq on tye same conditions. We also examined these effects in the presence of Torin-1, an inhibitor of mTOR

ORGANISM(S): Homo sapiens

PROVIDER: GSE66927 | GEO | 2015/11/04

SECONDARY ACCESSION(S): PRJNA278390

REPOSITORIES: GEO

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Ribo_seq (aka ribosome profiling) analysis of control and Myc-induced U2OS cells

Project description:We used Ribo-seq to examine the effect of Myc activation on protein translation in U2OS cells and correalted these changes with alterations in RNA level measured by RNA-seq on tye same conditions. We also examined these effects in the presence of Torin-1, an inhibitor of mTOR We measure ribosome occupancy profiles in U2OS cells containing an inducible Myc expression vector that were induced or mock-treated in duplicates for 36 hours. In addition, we repeated the experiments in the presence of Torin-1, an inhibitor of mTOR.

2015-11-04 | E-GEOD-66927 | biostudies-arrayexpress

RNA-seq analysis of control and Myc-induced U2OS cells

Project description:We used RNA-seq to examine the effect of Myc activation on U2OS cells transcriptome. We also examined these effects in the presence of Torin-1, an inhibitor of mTOR We measure gene expression profiles in U2OS cells containing an inducible Myc expression vector that were induced or mock-treated in duplicates for 36 hours. In addition, we repeated the experiments in the presence of Torin-1, an inhibitor of mTOR.

2015-11-04 | E-GEOD-66789 | biostudies-arrayexpress

RNA-seq analysis of control and Myc-induced U2OS cells

Project description:We used RNA-seq to examine the effect of Myc activation on U2OS cells transcriptome. We also examined these effects in the presence of Torin-1, an inhibitor of mTOR

2015-11-04 | GSE66789 | GEO

Proteome profiling upon Myc activation

Project description:The effect of Myc activation on the proteome was investigated in U2OS cells and proteome changes were combined with Ribo-seq, RNA-seq and GRO-seq analyses.

2015-11-09 | PXD002073 | Pride

Ribosome profiling and RNA sequencing of U2OS cells overexpressing myc

Project description:Ribosome profiling and RNA sequencing was performed on U2OS cells, either control or overexpressing myc.

2017-07-27 | GSE59819 | GEO

GRO-seq analysis of control and Myc-induced U2OS cells

Project description:We used GRO-seq to examine the effect of Myc activation on RNA transcription in U2OS cells. We measure in duplicates gene transcription rates in U2OS cells containing an inducible Myc expression vector that were induced or mock-treated in duplicates for 5 hours.

2015-11-04 | E-GEOD-66928 | biostudies-arrayexpress

GRO-seq analysis of control and Myc-induced U2OS cells

Project description:We used GRO-seq to examine the effect of Myc activation on RNA transcription in U2OS cells.

2015-11-04 | GSE66928 | GEO

MYC overexpression leads to increased chromatin interactions at superenhancers and MYC binding sites

Project description:The MYC oncogene encodes for the MYC protein and is frequently dysregulated across multiple cancer cell types, making it an attractive target for cancer therapy. MYC overexpression leads to MYC binding at active enhancers, resulting in a global transcriptional amplification of active genes. Since superenhancers are frequently dysregulated in cancer, we hypothesized that MYC preferentially invades into superenhancers and alters the cancer genome organization. To that end, we performed ChIP-seq, RNA-seq, 4C-seq and SIQHiC (Spike-in Quantitative Hi-C) on the U2OS osteosarcoma cell line with tetracycline-inducible MYC. MYC overexpression in U2OS cells modulated histone acetylation and increased MYC binding at superenhancers. SIQHiC analysis revealed increased global chromatin contact frequency, particularly at chromatin interactions connecting MYC binding sites at promoters and enhancers. Immunofluorescence staining showed that MYC molecules formed punctate foci at these transcriptionally active domains after MYC overexpression. These results demonstrate the accumulation of overexpressed MYC at promoter-enhancer hubs and suggest that MYC invades into enhancers through spatial proximity. At the same time, the increased protein-protein interactions may strengthen these chromatin interactions to increase chromatin contact frequency. CTCF siRNA knockdown in MYC overexpressed U2OS cells demonstrated that removal of architectural proteins can disperse MYC and abrogate the increase in chromatin contacts. By elucidating the chromatin landscape of MYC driven cancers, we can potentially target MYC associated chromatin interactions for cancer therapy.

2022-01-17 | GSE164777 | GEO

The polyamine-hypusine circuit controls an oncogenic translational program necessary for MYC-driven lymphomagenesis

Project description:MYC oncogenes are activated in broad spectrum of human malignancies and transcriptionally reprogram the genome to drive cancer cell growth. Given this it is unclear if targeting a single effector will have a therapeutic benefit. MYC activates the polyaminehypusine circuit, which post-translationally modifies the translation factor eIF5A. The hypusine axis has been proposed to suppress tumorigenesis. Here we report essential roles for hypusinated eIF5A in the development and maintenance of Myc-driven lymphoma, where loss of eIF5A hypusination abolishes malignant transformation. Mechanistically, integrating RNA-seq, Ribo-seq and proteomic analyses revealed that efficient translation of select targets is dependent upon eIF5A hypusination, including key regulators of G1 to S phase cell cycle progression. Notably, this circuit controls Myc’s proliferative response at several levels, and it is activated across multiple tumor types. These findings suggest the hypusine circuit as a therapeutic target for a broad spectrum of malignancies.

2024-01-26 | PXD031361 | Pride

Whole-genome CRISPR screen of etoposide-treated U2OS and U2OS p53KO cells, and RNAseq of U2OS cells incubated in media conditioned by etoposide-treated U2OS or U2OS p53KO cells.

Project description:CRISPR screen: U2OS or U2OS p53KO cells expressing Cas9 were transduced with a whole-genome library of CRISPR sgRNAs, then treated with either DMSO or etoposide. Differential sgRNA abundances were calculated for each condition and used to determine the effect of each single gene knockout on fitness and the drug-induced death rate. RNA-Seq: U2OS or U2OS p53KO cells were cultured with either DMSO or etoposide for 48 hours, and then U2OS cells were incubated in this conditioned media for 8 hours. RNA was collected and use to observe differential expression changes between conditions.

2023-05-17 | GSE232592 | GEO

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