Complex Interplay between the RUNX Transcription Factors and Wnt/β-Catenin Pathway in Cancer: A Tango in the Night
Kerri Sweeney1, Ewan R. Cameron2,*, and Karen Blyth1,3,*
1CRUK Beatson Institute, Garscube Estate, Glasgow G61 1BD, UK, 2Glasgow Veterinary School, University of Glasgow, Glasgow G61 1QH, UK, 3Institute of Cancer Sciences, University of Glasgow, Glasgow G61 1QH, UK
Received December 12, 2019; Accepted December 19, 2019.; Published online February 3, 2020.
© Korean Society for Molecular and Cellular Biology. All rights reserved.

Cells are designed to be sensitive to a myriad of external cues so they can fulfil their individual destiny as part of the greater whole. A number of well-characterised signalling pathways dictate the cell’s response to the external environment and incoming messages. In healthy, well-ordered homeostatic systems these signals are tightly controlled and kept in balance. However, given their powerful control over cell fate, these pathways, and the transcriptional machinery they orchestrate, are frequently hijacked during the development of neoplastic disease. A prime example is the Wnt signalling pathway that can be modulated by a variety of ligands and inhibitors, ultimately exerting its effects through the β-catenin transcription factor and its downstream target genes. Here we focus on the interplay between the threemember family of RUNX transcription factors with the Wnt pathway and how together they can influence cell behaviour and contribute to cancer development. In a recurring theme with other signalling systems, the RUNX genes and the Wnt pathway appear to operate within a series of feedback loops. RUNX genes are capable of directly and indirectly regulating different elements of the Wnt pathway to either strengthen or inhibit the signal. Equally, β-catenin and its transcriptional co-factors can control RUNX gene expression and together they can collaborate to regulate a large number of third party co-target genes.
Keywords: cancer, RUNX1, RUNX2, RUNX3, Wnt, β-catenin

Current Issue

31 January 2020 Volume 43,
Number 1, pp. 1~95

This Article

Cited By Articles
  • CrossRef (0)

Social Network Service

Indexed in

  • Science Central
  • CrossMark