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Multiplexed proteome dynamics profiling of HSP90 inhibitor 17-AAG

ABSTRACT: Investigation of proteostatic effects of HSP90 inhibition by 17-AAG and differentiation of maturation state dependent HSP90 requirements of proteins.

INSTRUMENT(S): Orbitrap Fusion Lumos, Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): T Cell

SUBMITTER: Maria Faelth Savitski

LAB HEAD: Marcus Bantscheff

PROVIDER: PXD008633 | Pride | 2018-04-05

REPOSITORIES: Pride

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	0231_F1_R1_P73995B01_TMT8.raw.gz	Raw
	0231_F1_R1_P73995B02_TMT8.raw.gz	Raw
	0231_F1_R1_P73995B03_TMT8.raw.gz	Raw
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Publications

Multiplexed Proteome Dynamics Profiling Reveals Mechanisms Controlling Protein Homeostasis.

Savitski Mikhail M MM Zinn Nico N Faelth-Savitski Maria M Poeckel Daniel D Gade Stephan S Becher Isabelle I Muelbaier Marcel M Wagner Anne J AJ Strohmer Katrin K Werner Thilo T Melchert Stephanie S Petretich Massimo M Rutkowska Anna A Vappiani Johanna J Franken Holger H Steidel Michael M Sweetman Gavain M GM Gilan Omer O Lam Enid Y N EYN Dawson Mark A MA Prinjha Rab K RK Grandi Paola P Bergamini Giovanna G Bantscheff Marcus M

Cell 20180315 1

Protein degradation plays important roles in biological processes and is tightly regulated. Further, targeted proteolysis is an emerging research tool and therapeutic strategy. However, proteome-wide technologies to investigate the causes and consequences of protein degradation in biological systems are lacking. We developed "multiplexed proteome dynamics profiling" (mPDP), a mass-spectrometry-based approach combining dynamic-SILAC labeling with isobaric mass tagging for multiplexed analysis of ...[more]

PMID: 29551266

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Multiplexed proteome dynamics profiling of HSP90 inhibitor 17-AAG in T-cells

Project description:Investigation of proteostatic effects of HSP90 inhibition by 17-AAG and differentiation of maturation state dependent HSP90 requirements of proteins in resting T-cells.

2018-05-02 | PXD008635 | Pride

Multiplexed proteome dynamics profiling of HSP90 inhibitor 17-AAG in anti-CD3 and anti-CD28 stimulated T-cells

Project description:Investigation of proteostatic effects of HSP90 inhibition by 17-AAG and differentiation of maturation state dependent HSP90 requirements of proteins in activated T-cells.

2018-05-02 | PXD008634 | Pride

Expression profiling of HSP90 inhibitor 17-AAG in anti-CD3 and anti-CD28 stimulated T-cells

Project description:Investigation of expression effects of HSP90 inhibition by 17-AAG of proteins in resting and activated T-cells.

2018-05-02 | PXD008627 | Pride

Expression data from human colonic cancer cell line SW480 and its acquired 17-AAG resistance cell line SW480-R

Project description:Heat shock protein 90 (HSP90) is a molecular chaperone required for the stability and function of many proteins. The chaperoning of oncoproteins by HSP90 enhances survival, growth and invasive potential of cancer cells. HSP90 inhibitors are promising new anticancer agents, in which the benzoquinone ansamycin 17-allylamino-17-demethoxygeldanamycin (17-AAG) is currently in clinical evaluation. However, the implications of acquired resistance to this class of drug remain largely unexplored. In the present study, we have generated isogenic human colonic cancer cell line SW480 that is resistant to 17-AAG by continued culturing in the compound. We used microarrays to detail the global programme of gene expression underlying the acquired resistance to 17-AAG in SW480 and SW480-R cell lines.

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Wee1 Inhibition sensitizes prostate cancer cells to Hsp90 inhibitor to activate the intrinsic apoptotic pathway

Project description:Heat shock protein 90 (Hsp90) is an essential evolutionarily conserved molecular chaperone in eukaryotes. Cancer cells rely on Hsp90 to chaperone activated oncoproteins, and its involvement in numerous signaling pathways makes it an attractive target for drug development. Surprisingly, however, the impact of Hsp90 inhibitors on cancer cells is most commonly cytostatic, and efforts to enhance the anti-tumor activity of Hsp90 inhibitors in the clinic remain a significant challenge. In this study, we show that dual inhibition of Wee1 tyrosine kinase and Hsp90 causes prostate cancer cells to undergo apoptosis. Gene-expression profiling revealed that induction of the intrinsic apoptotic pathway by this drug combination coincided with transcriptional down-regulation of Survivin and Wee1, an outcome not seen in cells treated separately with either agent. At the translational level, expression of these two proteins as well as activated Akt was completely abrogated. Similar results were obtained in prostate cancer xenografts. These data establish a novel therapeutic strategy to enhance the efficacy of Hsp90 inhibitors in prostate cancer, and they provide a mechanistic rationale for stimulating the pro-apoptotic activity of Hsp90 inhibitors. In order to explore the mechanism underlying the enhanced cell death caused by Wee1 inhibitorII and 17-AAG combination, we performed microarray analysis using PC3 cells treated with Wee1 inhibitorII alone, 17-AAG alone, or the two drugs in combination. There are 12 samples in total. There are three experimental replicate. Samples 1, 5 and 9 are control (C) (untreated PC3- prostate cancer cells). Samples 2, 6, and 10 are cells treated with Wee1 inhibitor II (W). Samples 3, 7, and 11 are treated with 17-AAG (A), (an Hsp90 inhibitor). Samples 4, 8, and 12 are treated with both Wee1 inhibitorII and 17-AAG (WA). Samples 5 was removed from our analysis due to weak signal.

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Native SEC-MS of the human HT29 colon adenocarcinoma cell line treated with the HSP90 inhibitor tanespimycin (17-AAG)

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2022-12-20 | PXD033459 | Pride

Drug combination of 17-AAG and Belinostat on MDA-MB-231 breast cancer cells

Project description:Breast cancer is the most common cancer that threatens women's health. While the strategy of drug combination can help to reduce adverse effects and to overcome the resistance of clinical treatment of single drug. In this work, we report the synergetic effect between a HSP90 inhibitor 17-AAG and a HDAC inhibitor Belinostat, on the triple-negative breast cancer MDA-MB-231 cells. The RNA-Seq data analysis showed that the most over-represented KEGG pathways in the combination group came from migration or invasion related genes, which were not observed in the differentially expressed genes after the treatment of 17-AAG or Belinostat alone.

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Multiplexed proteome dynamics profiling of Estradiol and SERMs

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Molecular Signature of response and potential pathways related to resistance to the HSP90 inhibitor, 17-AAG, in breast cancer.

Project description:We have done transcriptional profiling of 17-AAG treated (24h, 48H) breast cancer cell lines to understand the mechanisms of the drug action and indicate novel set of pharmacodynamic biomarkers of the drug response as well as of resistance Two-condition experiment, Untreated vs. Treated sensitive cells. Phenotype replicates: 8 untreated replicates, 14 treated replicates.

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Expression data from 17-AAG resistance cell line

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