Selective antagonism of cJun for cancer therapy

Andrew Brennan, James Leech, Neil Kad, Jody Mason

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)

Abstract

The activator protein-1 (AP-1) family of transcription factors modulate a diverse range of cellular signalling pathways into outputs which can be oncogenic or anti-oncogenic. The transcription of relevant genes is controlled by the cellular context, and in particular by the dimeric composition of AP-1. Here, we describe the evidence linking cJun in particular to a range of cancers. This includes correlative studies of protein levels in patient tumour samples and mechanistic understanding of the role of cJun in cancer cell models. This develops an understanding of cJun as a focal point of cancer-altered signalling which has the potential for therapeutic antagonism. Significant work has produced a range of small molecules and peptides which have been summarised here and categorised according to the binding surface they target within the cJun-DNA complex. We highlight the importance of selectively targeting a single AP-1 family member to antagonise known oncogenic function and avoid antagonism of anti-oncogenic function.
Original languageEnglish
Article number184
Number of pages1
JournalJournal of Experimental and Clinical Cancer Research
Volume39
Issue number1
DOIs
Publication statusPublished - 11 Sep 2020

Keywords

  • c-Jun
  • activator protein-1
  • transcriptional activator
  • basic leucine zipper
  • cancer
  • peptides
  • protein-protein interaction

Fingerprint

Dive into the research topics of 'Selective antagonism of cJun for cancer therapy'. Together they form a unique fingerprint.

Cite this