Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1999;43(4):288-95.
doi: 10.1002/(SICI)1097-0169(1999)43:4<288::AID-CM2>3.0.CO;2-Y.

Relationship between cell migration and cell cycle during the initiation of epithelial to fibroblastoid transition

Affiliations

Relationship between cell migration and cell cycle during the initiation of epithelial to fibroblastoid transition

C Bonneton et al. Cell Motil Cytoskeleton. 1999.

Abstract

The NBT-II rat bladder carcinoma cell line, which displays epithelial to mesenchymal transition or EMT in response to FGF-1 stimulation, was used to study the interrelationships between cell cycle and cell scattering and locomotion. Time-lapse video microscopy experiments were performed with asynchronous growing cells and lovastatin-arrested cells. FGF-1 stimulation induced cell movement in cells in all phases of the cell cycle, except G2 + M phase, in which cells did not respond to stimulation. The delay between cell stimulation and cell movement depended on the age of the cell at the beginning of cell stimulation: cells less than 4 h old when stimulated by FGF-1 had a 1-h delay whereas cells more than 4 h old had a 3-h delay. Cells stimulated before they were 4 h old were temporarily arrested in their cell cycle progression. Older cells underwent mitosis on schedule. Lovastatin-treated cells were shown to be synchronized in the G1 phase and to migrate simultaneously after FGF-1 stimulation. These results indicate that the G1 phase was a critical phase for FGF-1 induced cell migration during epithelial to fibroblastoid transition.

PubMed Disclaimer

Substances

LinkOut - more resources