Cyclin degradation for cancer therapy and chemoprevention

Sarah J. Freemantle, Xi Liu, Qing Feng, Fabrizio Galimberti, Steven Blumen, David Sekula, Sutisak Kitareewan, Konstantin H. Dragnev, Ethan Dmitrovsky

Research output: Contribution to journalReview articlepeer-review


Cancer is characterized by uncontrolled cell division resulting from multiple mutagenic events. Cancer chemoprevention strategies aim to inhibit or reverse these events using natural or synthetic pharmacologic agents. Ideally, this restores normal growth control mechanisms. Diverse classes of compounds have been identified with chemopreventive activity. What unites many of them is an ability to inhibit the cell cycle by specifically modulating key components. This delays division long enough for cells to respond to mutagenic damage. In some cases, damage is repaired and in others cellular damage is sufficient to trigger apoptosis. It is now known that pathways responsible for targeting G1 cyclins for proteasomal degradation can be engaged pharmacologically. Emergence of induced cyclin degradation as a target for cancer therapy and chemoprevention in pre-clinical models is discussed in this article. Evidence for cyclin D1 as a molecular pharmacologic target and biological marker for clinical response is based on experience of proof of principle trials.

Original languageEnglish (US)
Pages (from-to)869-877
Number of pages9
JournalJournal of Cellular Biochemistry
Issue number4
StatePublished - Nov 1 2007
Externally publishedYes


  • Cancer chemoprevention
  • Cancer therapy
  • Cyclins
  • ISG15-UBE1L
  • Proteasome
  • Proteolysis
  • Ubiquitin

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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