TCF transcription factors: Molecular switches in carcinogenesis

Jeroen Roose, Hans Clevers

Research output: Contribution to journalReview articlepeer-review

273 Citations (Scopus)


Although originally cloned as lymphoid transcription factors, members of the T-cell factor (Tcf) family are now well recognized as key activators/repressors in many developmental processes. Transcriptionally inert Tcf factors become potent transactivators upon interaction with the Wnt signaling product β-catenin or its Drosophila counterpart Armadillo. In contrast, Tcf proteins mediate repression when bound to members of the Groucho family of transcriptional repressors, CBP and CtBP. Recently, Tcf factors have been reported as tumor inducers, aberrantly activating their target genes as a result of elevated β-catenin levels in many types of cancer. These abnormal β-catenin levels are usually caused by stabilizing mutations in β-catenin itself or truncating mutations in the adenomatous polyposis coli (APC) tumor suppressor gene. In this review, we will give a chronological overview of the Tcf factors and the phenotypes of Tcf mutant mice, as well as Tcf-binding partners. We will discuss Tcf signaling upon interaction with different partners, resulting in activator and repressor roles of Tcf factors in the light of carcinogenic events.

Original languageEnglish
Pages (from-to)M23-M37
JournalBiochimica et Biophysica Acta - Reviews on Cancer
Issue number2-3
Publication statusPublished - 29 Oct 1999
Externally publishedYes


  • Adenomatous polyposis coli tumor suppressor gene
  • cAMP response element-binding- binding protein
  • Cancer
  • CtBP
  • Groucho
  • Mutation
  • T-cell factor/lymphoid enhancer factor expression
  • T-cell factor/lymphoid enhancer factor knock out mouse
  • T-cell factor/lymphoid enhancer factor transcription factor
  • Wnt signaling
  • β-Catenin


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