Mark A. White

TL;DR: It is demonstrated that androgens can co-opt the AMPK-PGC-1α signaling cascade, a known homeostatic mechanism, to increase prostate cancer cell growth.

TL;DR: The data suggest that androgen receptor (AR) signaling can promote prostate cancer through the upregulation of G6PD and therefore, the flux of sugars through the pentose phosphate pathway, and support a vital role for other metabolic pathways in prostate cancer cell growth and maintenance.

TL;DR: A functional role for increased autophagy in prostate cancer progression is demonstrated, a mechanism for how Autophagy is augmented is provided, and the potential of targeting this process for the treatment of advanced prostate cancer is highlighted.

TL;DR: Data indicate that three well-established oncogenic drivers (AR, MYC, and mTOR) function by converging to collectively increase the expression of glutamine transporters, thereby promoting glutamine uptake and subsequent prostate cancer cell growth.

TL;DR: Data demonstrate that prostate cancer cells can increase the functional levels of GLUT12 through multiple mechanisms to promote glucose uptake and subsequent cell growth.