Journal
BIOCHEMICAL SOCIETY TRANSACTIONS
Volume 40, Issue -, Pages 90-93Publisher
PORTLAND PRESS LTD
DOI: 10.1042/BST20110678
Keywords
Akt/protein kinase B (PKB); cancer metastasis; epithelial-mesenchymal transition (EMT); mitogen-activated protein kinase (MAPK); Twist phosphorylation; transforming growth factor beta receptor signalling (TGF beta R signalling)
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Funding
- Swiss National Science Foundation [SNF 31003A_130838]
- Swiss National Science Foundation (SNF) [31003A_130838] Funding Source: Swiss National Science Foundation (SNF)
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The transcription factor Twist plays vital roles during embryonic development through regulating/controlling cell migration. However, postnatally, in normal physiological settings, Twist is either not expressed or inactivated. Increasing evidence shows a strong correlation between Twist reactivation and both cancer progression and malignancy, where the transcriptional activities of Twist support cancer cells to disseminate from primary tumours and subsequently establish a secondary tumour growth in distant organs. However, it is largely unclear how this signalling programme is reactivated or what signalling pathways regulate its activity. The present review discusses recent advances in Twist regulation and activity, with a focus on phosphorylation-dependent Twist activity, potential upstream kinases and the contribution of these factors in transducing biological signals from upstream signalling complexes. The recent advances in these areas have shed new light on how phosphorylation-dependent regulation of the Twist proteins promotes or suppresses Twist activity, leading to differential regulation of Twist transcriptional targets and thereby influencing cell fate.
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