Targeting the E3 ubiquitin ligases DCAF15 and cereblon for cancer therapy

Semin Cancer Biol. 2020 Dec;67(Pt 2):53-60. doi: 10.1016/j.semcancer.2020.03.007. Epub 2020 Mar 18.

Abstract

Small molecule-mediated inhibition of protein function is the rational behind therapeutic efficacy of the majority clinically used drugs. In order for a drug to achieve pharmacologically relevant inhibition, efficient target engagement at high selectivity and specificity is necessary to obtain the desired therapeutic effect minimizing offtarget outcomes. Majority of small molecules approaches developed so far have failed in their attempt to reach clinical efficacy because of low selectivity and low specificity in achieving close to 100 % target inhibition. Recently, approaches that directly control cellular protein levels have opened the potential to accomplish a high grade of efficacy not imaginable with traditional small-molecule inhibitors. Research in this area has just started opening avenues to effectively degrade a cellular target of choice and will soon impact clinical efficacy.

Keywords: CRBN; Cereblon; Cullin-RING ligasem lymphoma; DCAF15; Molecular glue; Myeloma; PROTAC; Ubiquitin.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Adaptor Proteins, Signal Transducing / genetics
  • Adaptor Proteins, Signal Transducing / metabolism*
  • Antineoplastic Agents / pharmacology*
  • Hematologic Neoplasms / drug therapy
  • Humans
  • Immunologic Factors / pharmacology
  • Intracellular Signaling Peptides and Proteins / genetics
  • Intracellular Signaling Peptides and Proteins / metabolism*
  • Molecular Targeted Therapy / methods*
  • Ubiquitin-Protein Ligases / genetics
  • Ubiquitin-Protein Ligases / metabolism*

Substances

  • Adaptor Proteins, Signal Transducing
  • Antineoplastic Agents
  • CRBN protein, human
  • DCAF15 protein, human
  • Immunologic Factors
  • Intracellular Signaling Peptides and Proteins
  • Ubiquitin-Protein Ligases