PI-3 kinase p110β: a therapeutic target in advanced prostate cancers.
Prostate cancers in the castration-resistant stage are life-threatening because they are not curable in clinic. The novel androgen receptor inhibitor Xandi (Enzalutamide) and the new CYP17 inhibitor Zytiga (Abiraterone) prolonged patient survival only a few months in advanced prostate cancers. Therefore, novel therapeutic agents for advanced prostate cancers are urgently needed. PI-3 kinases are major intracellular signaling molecules that regulate multiple signal pathways related to cellular metabolism, cytokinesis, growth and survival. Accumulating evidence in the literature indicates that some isoforms of this kinase family are oncogenic and abnormally expressed in various human cancers, including prostate cancers. Recent extensive studies from our group and others showed that PI-3 kinase p110β is aberrantly overexpressed in advanced prostate cancers and is critical for prostate cancer development and progression as demonstrated in cell-based and animal models. Importantly, novel p110β-specific inhibitors have been developed and are currently been testing in clinical trials. In this article, we will briefly summarize recent developments in this regard.
Department of Urology, The University of Kansas Medical Center Kansas City, KS 66160, USA ; Department of Molecular & Integrative Physiology, The University of Kansas Medical Center Kansas City, KS 66160, USA ; Department of Pathology, Shaoxing People's Hospital Shaoxing 312000, China ; Department of Urology, Guangdong Medical College Zhanjiang 524001, China.
Benyi
B
Li
Department of Pathology, Shaoxing People's Hospital Shaoxing 312000, China.
Aijing
A
Sun
Department of Urology, Guangdong Medical College Zhanjiang 524001, China.
Wencong
W
Jiang
Department of Urology, The University of Kansas Medical Center Kansas City, KS 66160, USA.
J Brantley
JB
Thrasher
Department of Molecular & Integrative Physiology, The University of Kansas Medical Center Kansas City, KS 66160, USA.
Paul
P
Terranova
Prostate cancer; cancer therapy; castration resistance; p110β