Hypertonicity activates GSK3beta in tumor cells.
Responses to perturbations in the composition of the extracellular environment are crucial to maintain cell and tissue homeostasis. In hypertonic conditions cell lines derived from kidney epithelium initiate a variety of stress responses to maintain cell viability that include activation of Mitogen Activated Protein Kinases (MAPK). We previously showed that NaCl also regulates MAPK in different tumor cell lines and we now show that when hypertonic conditions induced with NaCl and other osmolytes were used to stimulate several tumor cell lines, Glycogen Synthase Kinase 3beta (GSK3beta) was rapidly dephosphorylated at serine 9 and its kinase activity was increased. This response was both time- and dose-dependent, it was independent of the Akt signaling pathway and did not increase steady state levels of phosphorylation of beta-catenin, although the data suggested that activated GSK3beta could regulate the activity of ERK1/2.
Perez-Pinera
Pablo
P
Departamento de Morfología y Biología Celular, Universidad de Oviedo, Oviedo, Spain. pab_correo@yahoo.com
Menendez-Gonzalez
Manuel
M
del Valle
Miguel
M
Vega
Jose Antonio
JA
D004789:Enzyme Activation / Q000187:drug effects; D038362:Glycogen Synthase Kinase 3 / Q000378:metabolism*; D000071679:Glycogen Synthase Kinase 3 beta; D006367:HeLa Cells; D006801:Humans; D006982:Hypertonic Solutions / Q000494:pharmacology; D009361:Neoplasm Invasiveness; D009369:Neoplasms / Q000201:enzymology* / Q000473:pathology*; D010766:Phosphorylation / Q000187:drug effects; D010768:Phosphoserine / Q000378:metabolism
D006982:Hypertonic Solutions; D010768:Phosphoserine; C000605506:GSK3B protein, human; D000071679:Glycogen Synthase Kinase 3 beta; D038362:Glycogen Synthase Kinase 3