Development of Mithramycin Analogues with Increased Selectivity toward ETS Transcription Factor Expressing Cancers

J Med Chem. 2018 Sep 13;61(17):8001-8016. doi: 10.1021/acs.jmedchem.8b01107. Epub 2018 Aug 28.

Abstract

Mithramycin A (1) was identified as the top potential inhibitor of the aberrant ETS transcription factor EWS-FLI1, which causes Ewing sarcoma. Unfortunately, 1 has a narrow therapeutic window, compelling us to seek less toxic and more selective analogues. Here, we used MTMSA (2) to generate analogues via peptide coupling and fragment-based drug development strategies. Cytotoxicity assays in ETS and non-ETS dependent cell lines identified two dipeptide analogues, 60 and 61, with 19.1- and 15.6-fold selectivity, respectively, compared to 1.5-fold for 1. Importantly, the cytotoxicity of 60 and 61 is <100 nM in ETS cells. Molecular assays demonstrated the inhibitory capacity of these analogues against EWS-FLI1 mediated transcription in Ewing sarcoma. Structural analysis shows that positioning the tryptophan residue in a distal position improves selectivity, presumably via interaction with the ETS transcription factor. Thus, these analogues may present new ways to target transcription factors for clinical use.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Antibiotics, Antineoplastic / chemistry
  • Antineoplastic Agents / chemistry*
  • Antineoplastic Agents / pharmacology*
  • Bone Neoplasms / drug therapy
  • Bone Neoplasms / metabolism
  • Bone Neoplasms / pathology
  • Cell Proliferation / drug effects*
  • Drug Development*
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Male
  • Molecular Structure
  • Oncogene Proteins, Fusion / antagonists & inhibitors*
  • Oncogene Proteins, Fusion / genetics
  • Oncogene Proteins, Fusion / metabolism
  • Plicamycin / analogs & derivatives*
  • Prostatic Neoplasms / drug therapy
  • Prostatic Neoplasms / metabolism
  • Prostatic Neoplasms / pathology
  • Proto-Oncogene Protein c-fli-1 / antagonists & inhibitors*
  • Proto-Oncogene Protein c-fli-1 / genetics
  • Proto-Oncogene Protein c-fli-1 / metabolism
  • Proto-Oncogene Proteins c-ets / antagonists & inhibitors*
  • Proto-Oncogene Proteins c-ets / genetics
  • Proto-Oncogene Proteins c-ets / metabolism
  • RNA-Binding Protein EWS / antagonists & inhibitors*
  • RNA-Binding Protein EWS / genetics
  • RNA-Binding Protein EWS / metabolism
  • Sarcoma, Ewing / drug therapy*
  • Sarcoma, Ewing / metabolism
  • Sarcoma, Ewing / pathology
  • Tumor Cells, Cultured

Substances

  • Antibiotics, Antineoplastic
  • Antineoplastic Agents
  • EWS-FLI fusion protein
  • Oncogene Proteins, Fusion
  • Proto-Oncogene Protein c-fli-1
  • Proto-Oncogene Proteins c-ets
  • RNA-Binding Protein EWS
  • Plicamycin