Altered SK3/KCa2.3-mediated migration in adenomatous polyposis coli (Apc) mutated mouse colon epithelial cells.
Lost of adenomatous polyposis coli gene (Apc) disturbs the migration of intestinal epithelial cells but the mechanisms have not been fully characterized. Since we have demonstrated that SK3/KCa2.3 channel promotes cancer cell migration, we hypothesized that Apc mutation may affect SK3/KCa2.3 channel-mediated colon epithelial cell motility. We report evidence that SK3/KCa2.3 channel promotes colon epithelial cells motility. Following Apc mutation SK3/KCa2.3 expression is largely reduced leading to a suppression of the SK3/KCa2.3 channel mediated-cell migration. Our findings reveal a previously unknown function of the SK3/KCa2.3 channel in epithelial colonic cells, and suggest that Apc is a powerful regulator SK3/KCa2.3 channel.
Potier
Marie
M
INSERM U921, Nutrition Croissance et Cancer, 10 Boulevard Tonnelle, Tours Cedex, France.
Tran
Truong An
TA
Chantome
Aurelie
A
Girault
Alban
A
Joulin
Virginie
V
Bougnoux
Philippe
P
Vandier
Christophe
C
Pierre
Fabrice
F
D025601:Adenomatous Polyposis Coli Protein / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D002460:Cell Line; D002465:Cell Movement; D003106:Colon / Q000166:cytology / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000166:cytology / Q000378:metabolism; D051379:Mice; D008817:Mice, Mutant Strains; D051640:Small-Conductance Calcium-Activated Potassium Channels
D025601:Adenomatous Polyposis Coli Protein; C496900:Kcnn3 protein, mouse; D051640:Small-Conductance Calcium-Activated Potassium Channels