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Related Experiment Video

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Different HSP90 Inhibitors Exert Divergent Effect on Myxoid Liposarcoma In Vitro and In Vivo.

Christoffer Vannas1,2, Lisa Andersson1, Soheila Dolatabadi1

  • 1Sahlgrenska Center for Cancer Research, Department of Laboratory Medicine, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, SE-405 30 Gothenburg, Sweden.

Biomedicines
|March 25, 2022
PubMed
Summary

Different HSP90 inhibitors show varied efficacy in treating myxoid liposarcoma (MLS). While some reduced tumor growth, one unexpectedly increased it, highlighting the need for careful selection in clinical trials.

Keywords:
HSP90 inhibitioncombination therapydrug treatmentmyxoid liposarcomareceptor tyrosine kinase signaling

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Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Therapeutic options for relapsed or metastatic myxoid liposarcoma (MLS) are limited, with no targeted therapies currently available.
  • Heat shock protein 90 (HSP90) inhibition is a potential therapeutic strategy for MLS, but clinical effects of different inhibitors vary.
  • No comparative studies on HSP90 inhibitors in MLS have been conducted.

Purpose of the Study:

  • To evaluate the efficacy of three HSP90 inhibitors (17-DMAG, AUY922, STA-9090) in MLS.
  • To compare their effects on MLS cell lines and a patient-derived xenograft (PDX) model.
  • To investigate their impact on key signaling pathways and combination effects with standard chemotherapeutics.

Main Methods:

  • In vitro assessment of MLS cell line growth inhibition by 17-DMAG, AUY922, and STA-9090.
  • In vivo evaluation using an MLS patient-derived xenograft (PDX) model.
  • Analysis of MAPK and PI3K/AKT signaling pathway activity and downstream effects.
  • Combination studies with trabectidin and doxorubicin.

Main Results:

  • All tested HSP90 inhibitors reduced in vitro MLS cell growth.
  • In vivo, 17-DMAG inhibited tumor growth, while AUY922 paradoxically increased tumor growth and aggressiveness.
  • 17-DMAG and STA-9090 decreased MAPK and PI3K/AKT signaling, whereas AUY922 caused ERK upregulation.
  • All inhibitors showed synergy with trabectidin but not doxorubicin.

Conclusions:

  • HSP90 inhibitors exhibit significantly different downstream effects and treatment outcomes in MLS, despite targeting the same protein.
  • The choice of HSP90 inhibitor is critical and requires careful consideration before clinical application in MLS and other cancers.
  • These findings underscore the importance of preclinical comparative studies to guide therapeutic strategies.