Figure 9.

A proposed scheme illustrating the distinct roles of AKT1/2 in ESCC and their modulation by oridonin. AKT is activated by upstream kinases. Receptor tyrosine kinase (RTK) or phosphatidylinositide 3-kinase (PI3-K) stimulates mTOR, GSK3β or NF-κB thereby promoting cell cycle, preventing apoptosis and increasing cell proliferation. Oridonin targets AKT and blocks the signals of downstream targets, therefore inducing cell cycle arrest and apoptosis as well as inhibiting cell proliferation.