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A Proteomic Platform Enables to Test for AML Normalization In Vitro.

Samuel M Meier-Menches1,2,3, Benjamin Neuditschko1,2, Lukas Janker1,3

  • 1Department of Analytical Chemistry, Faculty of Chemistry, University of Vienna, Vienna, Austria.

Frontiers in Chemistry
|February 18, 2022
PubMed
Summary

A new in vitro model using proteome profiling helps test cancer drug combinations. This study reveals how cancer cells adapt to treatments, aiding in the development of novel therapies for acute myeloid leukaemia (AML) and beyond.

Keywords:
AML—acute myeloid leukaemiaRutheniumarsenic trioxidecancerdifferentiationnormalizationplecstatin-1proteomics

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Area of Science:

  • Molecular Biology and Oncology
  • Proteomics and Cancer Therapeutics

Background:

  • Acute promyelocytic leukaemia (APL) is treatable with arsenic trioxide (ATO) and all-trans retinoic acid (ATRA), which induce differentiation and apoptosis.
  • Existing treatments lack in vitro models for evaluating novel differentiation inducers combined with metallopharmaceuticals.
  • Understanding cancer cell plasticity is crucial for developing effective combination therapies.

Purpose of the Study:

  • To establish an experimental framework using proteome profiling for evaluating combination treatments in acute myeloid leukaemia (AML) cell lines.
  • To characterize differentiation- and metal-specific effects of ATO and a novel metallopharmaceutical, plecstatin-1, in AML and APL models.
  • To investigate cancer cell cytoprotective plasticity as a predictor for therapeutic response.

Main Methods:

  • Proteome profiling was employed to analyze protein expression changes in AML (HL-60, U937) and APL (NB4) cell lines.
  • Cells were treated with arsenic trioxide (ATO) and the organoruthenium compound plecstatin-1, in combination with differentiation inducers.
  • Comparative analysis of cellular responses, including integrated stress response (ISR) and redox defense, was performed.

Main Results:

  • Differentiation significantly impacted the proteome, affecting approximately 10% of identified proteins in AML cell lines.
  • ATO induced distinct cytoprotective effects in HL-60 (ISR, redox defense) and U937 (proteasomal responses, metabolic rewiring) cells.
  • The APL cell line NB4 showed limited plasticity, lacking adaptive responses to ATO-induced stress, correlating with clinical efficacy.
  • Plecstatin-1 combination therapy mirrored ATO effects in HL-60 cells and showed limited plasticity in NB4 cells, suggesting potential beyond APL.

Conclusions:

  • The developed proteome profiling framework effectively characterizes differentiation and metal-specific effects of combination therapies in AML models.
  • Cancer cell cytoprotective plasticity is a key factor influencing treatment response, with limited plasticity in NB4 cells explaining ATO/ATRA success.
  • Plecstatin-1 represents a promising alternative to ATO, with potential therapeutic applications in APL and other cancers like U937, based on plasticity assessment.