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

ABSTRACT: 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.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Sergio Nasi

PROVIDER: E-GEOD-25039 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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