SGK1-dependent intestinal tumor growth in APC-deficient mice.

  title={SGK1-dependent intestinal tumor growth in APC-deficient mice.},
  author={Kan Wang and Shuchen Gu and Omaima Nasir and Michael F{\"o}ller and Teresa Felicitas Ackermann and Karin Klingel and Reinhard Kandolf and Dietmar Kuhl and Christos Stournaras and Florian Lang},
  journal={Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology},
  volume={25 2-3},
Adenomatous polyposis coli (APC) is inactivated in familial adenomatous polyposis and sporadic colorectal cancer. Mice carrying defective APC (apc(Min/+)) spontaneously develop gastrointestinal tumors. APC binds GSK3beta, which phosphorylates beta-catenin thus fostering its degradation. beta-catenin upregulates the serum- and glucocorticoid-inducible kinase Sgk1, which inhibits GSK3beta. The present study explored the role of SGK1 in tumor growth of apc(Min/+)mice. apc(Min/+)mice were crossed… CONTINUE READING
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