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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE227843 | GEO | 2023/04/09

REPOSITORIES: GEO

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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.

2023-04-09 | GSE227841 | GEO

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

2023-04-09 | GSE227842 | GEO

Effect of Omomyc on the in vitro growth of A375 human melanoma cell line

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 vitro in A375 (mutated in BRAF) melanoma cell line. We used microarrays to detail the change in the gene expression programs induced by Omomyc on day 4.

2023-04-09 | GSE227840 | GEO

BRAF activation by metabolic stress promotes glycolysis and survival, sensitizing NRASQ61 mutated melanomas to targeted therapy.

Project description:NRAS-mutated melanoma lacks an approved first-line treatment. Metabolic reprogramming is considered a novel target to control cancer; however, it is mostly unknow how the NRAS oncogene contributes to this cancer hallmark. Here, we show that NRASQ61-mutated melanomas harbor specific metabolic alterations that render cells sensitive to sorafenib upon metabolic stress. Mechanistically, these cells seem to depend on glucose metabolism, as glucose deprivation promotes the switch of the RAF isoform used from CRAF to BRAF. This process contributes to cell survival and sustains glucose metabolism through the phosphorylation of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 2/6- phosphofructo-2-kinase/fructose-2,6-bisphosph 3 (PFKFB2/PFKFB3) heterodimers by BRAF. In turn, this phosphorylation favors the allosteric activation of phosphofructokinase-1 (PFK1), generating a feedback loop linking glycolysis and the RAS signaling pathway. In vivo treatment of NRASQ61 mutant melanomas, including patient-derived xenografts, with the combination of 2-deoxy-D-glucose (2-DG) and sorafenib effectively inhibits tumor growth. Thus, we provide evidence of the contributions of NRAS oncogenes to metabolic rewiring and proof of principle for the treatment of NRAS-mutated melanoma with combinations of metabolic stress (glycolysis inhibitors) and already approved drugs such as sorafenib.

2023-01-09 | PXD028297 | Pride

Individualized surgery: gamma-probe-guided lymphadenectomy in patients with clinically enlarged lymph node metastases from melanomas.

Project description: Not available

| S-EPMC3618405 | biostudies-other

Whole transcriptome analysis of T11 treated with FPP-1746-Omomyc

Project description:RNA Sequencing of claudin-low triple negative breast cancer cells T11 treated with FPP-1746-Omomyc, Omomyc, FPP-1746 and vehicle control (PBS) to determine differentially regulated genes induced by FPP-1746-Omomyc

2020-09-26 | GSE104553 | GEO

Deep Inguinal Lymph Node Metastases Can Predict Pelvic Lymph Node Metastases and Prognosis in Penile Squamous Cell Carcinoma.

Project description: Not available

| S-EPMC8479104 | biostudies-literature

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.

2010-12-21 | E-GEOD-25039 | biostudies-arrayexpress

Effect of Omomyc treatment on MYC mediated transcription

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

2019-09-01 | GSE131075 | GEO

RNA-seq analysis identifies different transcriptomic types and developmental trajectories of primary melanomas

Project description:Recent studies revealed trajectories of mutational events in early melanomagenesis, but the accompanying changes in gene expression are far less understood. Therefore, we performed a comprehensive RNA-Seq analysis of laser-microdissected melanocytic nevi (n=23) and primary melanoma samples (n=57) and characterized the molecular mechanisms of early melanoma development. Using self-organizing maps, unsupervised clustering and analysis of pseudotime (PT) dynamics to identify evolutionary trajectories, we describe here two transcriptomic types of melanocytic nevi (N1 and N2) and primary melanomas (M1 and M2). N1/M1 lesions are characterized by pigmentation-type and MITF gene signatures, and a high prevalence of NRAS mutations in M1 melanomas. N2/M2 lesions are characterized by inflammatory-type and AXL gene signatures with an equal distribution of wild type and mutated BRAF and low prevalence of NRAS mutations in M2 melanomas. Interestingly, N1 nevi and M1 melanomas and N2 nevi and M2 melanomas, respectively, cluster together, but there is no clustering in a stage-dependent manner. Transcriptional signatures of M1 melanomas harbour signatures of BRAF/MEK inhibitor resistance and M2 melanomas harbour signatures of anti-PD-1 antibody treatment resistance. Transcriptomic signatures suggest that the epigenetic regulators SMARCA2 and SMARCA4 are differentially involved in the epigenetic programming of the two melanoma types. Pseudotime dynamics of nevus and melanoma samples reflect a switch-like immune-escape mechanism in melanoma development with downregulation of immune genes paralleled by an increasing expression of a cell cycle signature in late-stage melanomas. Taken together, the transcriptome analysis identifies gene signatures and mechanisms underlying development of melanoma in early and late stages with relevance for diagnostics and therapy.

2018-07-19 | GSE112509 | GEO

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