Cross‐talk between AMPK and GSK3beta or CSK in selenium‐ or EGCG‐treated hepato‐carcinoma cells

AMP‐activated protein kinase (AMPK) activators control cancer cell proliferation, and It has been shown that AMPK acts as a negative regulator of cancer cell survival signals such as mTOR and Akt. In this study, the interrogation of GSK3β, a major target of Wnt or CSK and anti‐cancer regulator AMPK was explored in selenium or EGCG treated hepato‐carcinoma cells. Anti‐proliferating effect of selenium was achieved by the activation of AMPK, and dephosphorylation of GSK3β which resulted in the inhibition of β‐catenin translocation into nucleus. The application of AMPK siRNA or Compound C (AMPK inhibitor) supported the evidence that AMPK acts as an upstream signal of GSK3β or CSK. However, there exists a possibility of GSK3β or CSK to send feedback signals to AMPK. This study supports the strategy of applying selenium or EGCG in hepato‐carcinoma cells to activate AMPK as well as to modulate Wnt or CSK signaling pathways. [This work was supported by the Korea Science and Engineering Foundation (KOSEF) grant funded by the Korea government (MEST) (NO. R01‐2008‐000‐20131‐0)] Grant Funding Source : Minority Travel Awards