Abstract
Deregulation of the PI3K-Akt-mTOR pathway plays a critical role in the development and progression of many cancers. In prostate cancer, evidence suggests that it is mainly driven by PTEN loss of function. For many years, the development of selective Akt inhibitors has been challenging. In recent phase II and III clinical trials, Ipatasertib and Capivasertib associated with androgen deprivation therapies showed promising outcomes in patients with metastatic castration-resistant prostate cancer and PTEN-loss. Ongoing trials are currently assessing several Akt inhibitors in prostate cancer with different combinations, at different stages of the disease.
Highlights
IntroductionKnown as protein kinase B (PKB), is at the crossroads of several signalling pathways
Several of the proteins involved in the phosphoinositide 3-kinase (PI3K)-Akt-Mammalian target of rapamycin (mTOR) signalling pathway can function, when overexpressed, as oncoproteins, while the ones involved in quenching this pathway act as tumour suppressors
Its deregulation has been shown to play a critical role in many cancers, through PTEN
Summary
Known as protein kinase B (PKB), is at the crossroads of several signalling pathways. This protein plays a critical role in regulating diverse cellular functions including cell metabolism, proliferation, apoptosis suppression and angiogenesis. The upregulation of Akt has been reported in a variety of human malignancies, including digestive, neurological, gynaecological, and urological. Med. 2022, 11, 160 variety of human malignancies, including digestive, neurological, gynaecological, and cancers [2].cancers. Akt promotes cell survival proliferation throughthrough its effects the cellular urological [2]. Akt promotes cell and survival and proliferation its on effects on the cellular growth factors and inhibitsthrough apoptosis the inactivation of pro-apopgrowth factors and inhibits apoptosis thethrough inactivation of pro-apoptotic proteins [3].
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