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Effect of Omomyc treatment on MYC mediated transcription

ABSTRACT: Purpose: Identify MYC sensitive enes that are affected by treatment with Omomyc

ORGANISM(S): Homo sapiens

PROVIDER: GSE131075 | GEO | 2019/09/01

REPOSITORIES: GEO

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Effect of Omomyc treatment on MYC mediated transcription

Project description:Effect of Omomyc treatment on MYC mediated transcription

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OmoMYC blunts promoter invasion by oncogenic MYC to inhibit gene expression characteristic of MYC-dependent tumors

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2016-10-18 | GSE77328 | GEO

Transcriptional response to serum stimulation of Rat1 fibroblasts in the presence or absence of the Myc interfering molecule termed Omomyc.

Project description:Myc is a multifaceted bHLHZip transcription factor deregulated in the majority of human cancers. How to target Myc for cancer therapy is unclear, given its involvement in a variety of key functions in healthy cells. We used microarrays to capture the cellular transcriptional response to Omomyc – a Myc interfering molecule acting at the level of protein protein interactions that demonstrated a remarkable therapeutic efficacy in transgenic mouse cancer models. We found that Omomyc differently affects Myc induced gene repression and activation, channelling the Myc interactome activity to repression. To determine whether Omomyc causes widespread changes of the cell transcriptome, we analysed the transcriptional response to serum stimulation of Rat1 fibroblasts stably infected with an Omomer – Omomyc fused to the tamoxifen inducible oestrogen receptor ERTM – producing retrovirus (Rat1_Omomer) as compared to Rat1 cells infected with a control virus (Rat1_Control). Endogenous c-Myc is known to be sharply induced by serum and is critical for cell cycle re-entry. Cells were grown, serum-starved for 48 h in presence of tamoxifen (4-OHT) and stimulated by addition of fresh serum. Total RNA was collected from Rat1_Control and Rat1-Omomer cells at the time of serum re-addition (T0) and 90' thereafter (T90'), in the presence of tamoxifen.

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Effect of Omomyc on lymph node metastases from melanomas [SkMel147]

Project description:Skin melanomas are highly aggressive and metastatic. Omomyc is the best MYC inhibitor currently available. We analysed the effect of Omomyc expression in a transgenic and inducible (upon Doxycycline addition) manner in spontaneous lymph node metastases from SkMel147 (mutated in NRAS) melanoma cells in vivo. We used microarrays to detail the change in the gene expression programs induced by Omomyc on day 2.

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Effect of Omomyc on the in vivo growth of melanomas

Project description:Skin melanomas are highly aggressive and metastatic. Omomyc is the best MYC inhibitor currently available. We analysed the effect of Omomyc expression in a transgenic and inducible (upon Doxycycline addition) manner in melanoma cells in vivo in two different melanoma cell lines: A375 (mutated in BRAF), SkMel147 (mutated in NRAS). We used microarrays to detail the change in the gene expression programs induced by Omomyc on day 7.

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Effect of Omomyc on the in vivo growth of melanomas [SkMel147]

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Project description:MYC deregulation is common in human cancer and has a role in sustaining the aggressive cancer stem cell populations. MYC mediates a broad transcriptional response controlling normal biological programs but its activity is not clearly understood. We address MYC function in cancer stem cells through the inducible expression of Omomyc – a MYC derived polypeptide interfering with MYC activity – taking as model the most lethal brain tumor, glioblastoma. Omomyc bridles the key cancer stem-like cell features and affects tumor microenvironment, inhibiting angiogenesis. This occurs because Omomyc interferes with proper Myc localization and binds to DNA, with a preference for sites previously occupied by MYC. This is accompanied by (leads to) selective repression of master transcription factors for glioblastoma stem-like cell identity like POU3F2, SOX2, and OLIG2, upregulation of effectors of tumor suppression and differentiation such as PTEN, ID4, MIAT, and modulation of the expression of microRNAs that target molecules implicated in glioblastoma growth and invasion like EGFR and ZEB1. Data support a novel view of MYC as a network stabilizer that strengthens the regulatory nodes of the gene expression programs controlling cell phenotype and highlight Omomyc as model molecule for targeting cancer stem cells.

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Transcriptional response to serum stimulation of Rat1 fibroblasts in the presence or absence of the Myc interfering molecule termed Omomyc.

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Project description:Analysis of MDAMB231 cells treated with 12.8 µM Omomyc or vehicle (PBS) for three days.

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