Circadian patterns of growth factor receptor-dependent signaling and implications for carcinogenesis

Cell Commun Signal. 2024 Jun 10;22(1):319. doi: 10.1186/s12964-024-01676-w.


Several different signaling pathways that regulate cell proliferation and differentiation are initiated by binding of ligands to cell-surface and membrane-bound enzyme-linked receptors, such as receptor tyrosine kinases and serine-threonine kinases. They prompt phosphorylation of tyrosine and serine-threonine residues and initiate downstream signaling pathways and priming of intracellular molecules that convey the signal in the cytoplasm and nucleus, with transcriptional activation of specific genes enriching cell growth and survival-related cascades. These cell processes are rhythmically driven by molecular clockworks endowed in every cell type and when deregulated play a crucial role in cancer onset and progression. Growth factors and their matching receptor-dependent signaling are frequently overexpressed and/or dysregulated in many cancer types. In this review we focus on the interplay between biological clocks and Growth Factor Receptor-dependent signaling in the context of carcinogenesis.

Keywords: Biological clock; Cancer; Circadian; Growth factors; Ligand; Receptors.

Publication types

  • Review

MeSH terms

  • Animals
  • Carcinogenesis* / genetics
  • Carcinogenesis* / metabolism
  • Carcinogenesis* / pathology
  • Circadian Rhythm / genetics
  • Circadian Rhythm / physiology
  • Humans
  • Neoplasms / genetics
  • Neoplasms / metabolism
  • Neoplasms / pathology
  • Receptors, Growth Factor / metabolism
  • Signal Transduction*


  • Receptors, Growth Factor