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Response of Blastocladiella emersonii to hypoxia, iron deprivation and geldanamycin treatment followed by hypoxia.

ABSTRACT: Due to its aquatic saprophytic lifestyle, the fungus Blastocladiella emersonii seems to be adapted to low aerated environments and thus can be an interesting model of study of the hypoxic stress response. Iron deprivation, a hypoxia-mimicking stimulus due to HIF-1 stabilization, and geldanamycin, that causes HIF-1 depletion by HSP90 inhibition, are helpful parameters to find an evidence of an oxygen-dependent regulatory mechanism in B. emersonii similar to the metazoan HIF-1 pathway.

ORGANISM(S): Blastocladiella emersonii

PROVIDER: GSE17524 | GEO | 2009/08/07

SECONDARY ACCESSION(S): PRJNA118805

REPOSITORIES: GEO

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Response of Blastocladiella emersonii to hypoxia, iron deprivation and geldanamycin treatment followed by hypoxia.

Project description:Due to its aquatic saprophytic lifestyle, the fungus Blastocladiella emersonii seems to be adapted to low aerated environments and thus can be an interesting model of study of the hypoxic stress response. Iron deprivation, a hypoxia-mimicking stimulus due to HIF-1 stabilization, and geldanamycin, that causes HIF-1 depletion by HSP90 inhibition, are helpful parameters to find an evidence of an oxygen-dependent regulatory mechanism in B. emersonii similar to the metazoan HIF-1 pathway. Direct transcript comparison between cells grown under normoxic conditions (70%sat. O2 in air) and cells submitted to oxygen deprivation (direct and gradual) and iron (II) deprivation. It was also compared transcripts of cells submitted to direct 1-hour hypoxia (1%sat. O2) with cells treated with geldanamycin for 1 hour, followed to 1-hour hypoxia (1%sat. O2). There are at least 3 biological replicates (independent harvest) and 2 technical replicates of each array (L - left and R - right).

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Expression data analyzed with LPIA in A549 lung carcinoma cells treated with geldanamycin.

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Identification of 17-DMAG as a novel KDM4B inhibitor for combination therapy [RNA-seq]

Project description:Histone lysine demethylases (KDMs) are emerging as therapeutic targets in cancer. Development of potent KDM inhibitors may provide additional options for epigenomics-oriented therapies. Using a Time-Resolved Fluorescence Resonance Energy Transfer (TR-FRET) functional demethylation assay, in combination with a high-content immunofluorescence imaging phenotypic screen, Matrix-Assisted Laser Desorption/Ionization- Fourier Transform Ion Cyclotron Resonance mass spectrometry (MALDI-FTICR MS) and Amplified Luminescent Proximity Homogeneous Assay (ALPHA), we identified geldanamycin, an inhibitor of heat shock protein 90 (Hsp90), as a novel inhibitor of JmjC-domain containing demethylases such as KDM4B. We further found that geldanamycin can destabilize the PAX3-FOXO1 fusion oncoprotein, an Hsp90 client, which is a driver of clinically unfavorable alveolar rhabdomyosarcoma (aRMS). We then hypothesized that dual inhibition of PAX3-FOXO1 and epigenetic modifiers of aRMS would have synergistic antitumor activity. We repurposed the geldanamycin analog 17-DMAG to target aRMS and found that 17-DMAG significantly delays tumor growth , extends survival in xenograft mouse models, and inhibits expression of PAX3-FOXO1 targets and multiple oncogenic pathways including MYC, E2F and NOTCH. In addition, the combination of 17-DMAG with conventional chemotherapy or the bromodomain inhibitor JQ1 significantly enhances therapeutic efficacy. In summary, we have identified geldanamycin and 17-DMAG as dual KDM/Hsp90 inhibitors and 17-DMAG is efficacious against PAX3-FOXO1-driven rhabdomyosarcoma.

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