E2F1 as a target: promoter-driven suicide and small molecule modulators.

Abstract

Decreased requirements for mitogens and diminished sensitivity to antiproliferative signals are among the hallmarks of human cancer. These attributes are due, at least partly, to mutations that directly or indirectly compromise the function of the retinoblastoma tumor suppressor protein (pRB), which is a negative regulator of a family of cell-cycle regulatory transcription factors referred to generically as E2F. Activation of E2F target genes is sufficient to induce unscheduled cellular proliferation but, under certain circumstances, can also lead to programmed cell death (apoptosis). This chapter will review the role of E2F in cancer and outline opportunities for the development of anticancer agents based on E2F biology.

• Authors: William G Kaelin Jr
• Journal: Cancer biology & therapy (Cancer Biol Ther) 2003 Jul-Aug Vol. 2 Issue 4 Suppl 1 Pg. S48-54 ISSN: 1538-4047 [Print] United States
• PMID: 14508080 (Publication Type: Journal Article, Review)

Chemical References

• Antineoplastic Agents
• Cell Cycle Proteins
• DNA-Binding Proteins
• E2F Transcription Factors
• E2F1 Transcription Factor
• E2F1 protein, human
• Retinoblastoma Protein
• Transcription Factors

Topics

• Antineoplastic Agents (pharmacology)
• Cell Cycle Proteins
• DNA-Binding Proteins
• E2F Transcription Factors
• E2F1 Transcription Factor
• Humans
• Models, Biological
• Mutation
• Neoplasms (genetics, metabolism)
• Retinoblastoma Protein (genetics)
• Transcription Factors (agonists, antagonists & inhibitors, genetics, physiology)