Abstract
Junction-mediating and regulatory protein (JMY) is a novel p53 cofactor that regulates p53 activity during stress. JMY interacts with p300/CBP, which are ubiquitous transcriptional co-activators that interact with a variety of sequence-specific transcription factors, including hypoxia-inducible factor-1α (HIF-1α). In addition, JMY is an actin-nucleating protein, which, through its WH2 domains, stimulates cell motility. In this study, we show that JMY is upregulated during hypoxia in a HIF-1α-dependent manner. The JMY gene contains HIF-responsive elements in its promoter region and HIF-1α is recruited to its promoter during hypoxia. HIF-1α drives transcription of JMY, which accounts for its induction under hypoxia. Moreover, the enhanced cell motility and invasion that occurs during hypoxia requires JMY, as depleting JMY under hypoxic conditions causes decreased cell motility. Our results establish the interplay between JMY and HIF-1α as a new mechanism that controls cell motility under hypoxic stress.
DOI
10.1038/onc.2011.188
Publication Date
2011-12-01
Publication Title
Oncogene
Volume
30
Issue
48
Publisher
Springer Science and Business Media LLC
ISSN
1476-5594
Embargo Period
2024-11-19
First Page
4835
Last Page
4842
Recommended Citation
Coutts, A., Pires, I., Weston, L., Buffa, F., & et al. (2011) 'Hypoxia-driven cell motility reflects the interplay between JMY and HIF-1α', Oncogene, 30(48), pp. 4835-4842. Springer Science and Business Media LLC: Available at: https://doi.org/10.1038/onc.2011.188
