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. Author manuscript; available in PMC: 2010 Dec 1.
Published in final edited form as: Cancer Res. 2009 Nov 17;69(23):8967–8976. doi: 10.1158/0008-5472.CAN-09-2190

Fig. 4. Involvement of FBXW7 (A) and GSK3 (B) in perifosine-induced degradation of several proteins in the mTOR axis and a schematic model for the possible mechanism underlying the process (C).

Fig. 4

A, The given cell lines were treated with the indicated concentrations of perifosine for 24 h. B, H460 cells were pretreated with 50 mM LiCl or 20 µM SB216763 for 30 min and then co-treated with 10 µM perifosine for an additional 5 h. After the aforementioned treatments, the cells were then harvested for preparation of whole cell protein lysates and subsequent Western blot analysis. C, Hypothetic model for involvement of FBXW7 and GSK3 in perifosine-induced degradation of several proteins in the mTOR axis. Perifosine inhibits Akt, resulting in GSK3 activation, which phosphorylates mTOR and facilitates ubiquitination and degradation of mTOR by FBWX7. As a consequence, mTOR complexes will be destabilized and proteins associated with these complexes will be degraded.