Many cellular processes in cancer are attributed to kinase abnormal overexpression or activation of AKT has been signaling networks. V-akt murine thymoma viral oncogene observed in many cancers, including ovarian, lung, and pan-homolog (AKT) plays a major role in the PI3K/AKT signaling creatic cancers, and is associated with increased cancer cell pathways. AKT is activated by PI3K or phosphoinositide-proliferation and survival. Therefore, targeting AKT could dependent kinases (PDK) as well as growth factors, inflam-provide an important approach for cancer prevention and mation, and DNA damage. Signal transduction occurs through therapy. In this review, we discuss the rationale for targeting downstream effectors such as mTOR, glycogen synthase kinase AKT and also provide details regarding synthetic and natural 3 beta (GSK3b), or forkhead box protein O1 (FOXO1). The AKT-targeting compounds and their associated studies.
Bibliographical noteFunding Information:
This work was supported by grants from the NIH (CA187027, CA166011, CA196639), Key Program of Henan Province, China (grant no. 161100510300 to Z. Dong), the National Natural Science Foundation of China (NSFC81672767 to M.-H. Lee), and Henan Provincial Government, China.