English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Malfunctions of circadian clock trigger abnormal cellular processes and influence tumorigenesis. Using an  in vitro  and  in vivo  xenograft model, we show that circadian clock disruption via the downregulation of the core-clock genes  BMAL1 ,  PER2 , and  NR1D1  impacts the circadian phenotype of  MYC ,  WEE1 , and  TP53 , and affects proliferation, apoptosis, and cell migration. In particular, both our  in vitro  and  in vivo  results suggest an impairment of cell motility and a reduction in micrometastasis formation upon knockdown of  NR1D1 , accompanied by altered expression levels of  SNAI1  and  CD44 . Interestingly we show that differential proliferation and reduced tumour growth  in vivo  may be due to the additional influence of the host-clock and/or to the 3D tumour architecture. Our results raise new questions concerning host–tumour interaction and show that core-clock genes are involved in key cancer properties, including the regulation of cell migration and invasion by  NR1D1  in zebrafish xenografts.

The Core-Clock Gene NR1D1 Impacts Cell Motility In Vitro and Invasiveness in a Zebrafish Xenograft Colon Cancer Model