A natural-like synthetic small molecule impairs bcr-abl signaling cascades and induces megakaryocyte differentiation in erythroleukemia cells

PLoS One. 2013;8(2):e57650. doi: 10.1371/journal.pone.0057650. Epub 2013 Feb 27.

Abstract

Over the past years, we synthesized a series of new molecules that are hybrids of spirocyclic ketones as complexity-bearing cores with bi- and ter-phenyls as privileged fragments. Some of these newly-shaped small molecules showed antiproliferative, pro-apoptotic and differentiating activity in leukemia cell lines. In the present study, to investigate more in depth the mechanisms of action of these molecules, the protein expression profiles of K562 cells treated with or without the compounds IND_S1, MEL_T1, IND_S7 and MEL_S3 were analyzed using two-dimensional gel electrophoresis coupled with mass spectrometry. Proteome comparisons revealed several differentially expressed proteins, mainly related to cellular metabolism, chaperone activity, cytoskeletal organization and RNA biogenesis. The major results were validated by Western blot and qPCR. To attempt integrating findings into a cellular signaling context, proteomic data were explored using MetaCore. Network analysis highlighted relevant relationships between the identified proteins and additional potential effectors. Notably, qPCR validation of central hubs showed that the compound MEL_S3 induced high mRNA levels of the transcriptional factors EGR1 and HNF4-alpha; the latter to our knowledge is reported here for the first time to be present in K562 cells. Consistently with the known EGR1 involvement in the regulation of differentiation along megakaryocyte lineage, MEL_S3-treated leukemia cells showed a marked expression of glycoprotein IIb/IIIa (CD41) and glycoprotein Ib (CD42), two important cell markers in megakaryocytic differentiation, together with morphological aspects of megakaryoblasts and megakaryocytes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Biomarkers, Tumor / metabolism
  • Cell Differentiation / drug effects*
  • Cell Differentiation / genetics
  • Cell Shape / drug effects
  • Cluster Analysis
  • Fusion Proteins, bcr-abl / metabolism*
  • Gene Expression Regulation, Leukemic / drug effects
  • Humans
  • K562 Cells
  • Leukemia, Erythroblastic, Acute / genetics
  • Leukemia, Erythroblastic, Acute / pathology*
  • Megakaryocytes / drug effects
  • Megakaryocytes / metabolism
  • Megakaryocytes / pathology*
  • Multivariate Analysis
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / metabolism
  • Proteome / metabolism
  • Proteomics
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Reproducibility of Results
  • Signal Transduction / drug effects*
  • Signal Transduction / genetics
  • Small Molecule Libraries / chemistry
  • Small Molecule Libraries / pharmacology*
  • Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization

Substances

  • Biomarkers, Tumor
  • Neoplasm Proteins
  • Proteome
  • RNA, Messenger
  • Small Molecule Libraries
  • Fusion Proteins, bcr-abl

Grants and funding

This work was supported by a PRIN2009 Project Grant from MiUR, Italy. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.