RAC1 activity and intracellular ROS modulate the migratory potential of MCF-7 cells through a NADPH oxidase and NF kappa B-dependent mechanism
In the present study, we demonstrated that changes in Rac1 activity associated with the production of intracellular ROS modulate the migratory properties in MCF-7 and T47D human mammary cell lines. We also described that the NFÎºB pathway exerts a downstream control on the expression of the ROS-dependent cellular migratory potential. These results emphasize the importance of redox balance in the acquisition of malignancy and support previous data sustaining that an oxidative environment predisposes cells to activate signal-transduction pathways actively involved in cellular oncogenesis. Our data also provides evidence that NADPH oxidase could constitute the main source of intracellular ROS in response to changes in Rac1 activity. We suggest that Rac1 plays a role in cellular migration not only limited to its known function in reorganization of the actin cytoskeleton, but also as part of the intracellular machinery that controls the redox balance. Â© 2008 Elsevier Ireland Ltd. All rights reserved.
|Título según WOS:||RAC1 activity and intracellular ROS modulate the migratory potential of MCF-7 cells through a NADPH oxidase and NF kappa B-dependent mechanism|
|Título según SCOPUS:||RAC1 activity and intracellular ROS modulate the migratory potential of MCF-7 cells through a NADPH oxidase and NF?B-dependent mechanism|
|Título de la Revista:||CANCER LETTERS|
|Fecha de publicación:||2008|
|Página de inicio:||125|