The Mechanism of Action of Unique Small Molecules that Inhibit the Pim Protein Kinase Blocking Prostate Cancer Cell Growth

2010 ◽  
Author(s):  
Andrew S. Kraft
Keyword(s):  
Prostate Cancer ◽  
Protein Kinase ◽  
Cell Growth ◽  
Small Molecules ◽  
Cancer Cell ◽  
Mechanism Of Action ◽  
Prostate Cancer Cell ◽  
Cancer Cell Growth

scholarly journals AMP-activated protein kinase promotes human prostate cancer cell growth and survival

2009 ◽  
Vol 8 (4) ◽  
pp. 733-741 ◽  
Author(s):  
Hyeon Ung Park ◽  
Simeng Suy ◽  
Malika Danner ◽  
Vernon Dailey ◽  
Ying Zhang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Protein Kinase ◽  
Cell Growth ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Human Prostate Cancer ◽  
Cancer Cell Growth ◽  
Human Prostate Cancer Cell ◽  
Growth And Survival ◽  
Amp Activated Protein Kinase

scholarly journals GLUT12 promotes prostate cancer cell growth and is regulated by androgens and CaMKK2 signaling

2018 ◽  
Vol 25 (4) ◽  
pp. 453-469 ◽  
Author(s):  
Mark A White ◽  
Efrosini Tsouko ◽  
Chenchu Lin ◽  
Kimal Rajapakshe ◽  
Jeffrey M Spencer ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Plasma Membrane ◽  
Protein Kinase ◽  
Cell Growth ◽  
Glucose Uptake ◽  
Cancer Cell ◽  
Glucose Transporter ◽  
Prostate Cancer Cell ◽  
Cancer Cell Growth ◽  
Ampk Signaling

Despite altered metabolism being an accepted hallmark of cancer, it is still not completely understood which signaling pathways regulate these processes. Given the central role of androgen receptor (AR) signaling in prostate cancer, we hypothesized that AR could promote prostate cancer cell growth in part through increasing glucose uptake via the expression of distinct glucose transporters. Here, we determined that AR directly increased the expression ofSLC2A12, the gene that encodes the glucose transporter GLUT12. In support of these findings, gene signatures of AR activity correlated withSLC2A12expression in multiple clinical cohorts. Functionally, GLUT12 was required for maximal androgen-mediated glucose uptake and cell growth in LNCaP and VCaP cells. Knockdown of GLUT12 also decreased the growth of C4-2, 22Rv1 and AR-negative PC-3 cells. This latter observation corresponded with a significant reduction in glucose uptake, indicating that additional signaling mechanisms could augment GLUT12 function in an AR-independent manner. Interestingly, GLUT12 trafficking to the plasma membrane was modulated by calcium/calmodulin-dependent protein kinase kinase 2 (CaMKK2)-5′-AMP-activated protein kinase (AMPK) signaling, a pathway we previously demonstrated to be a downstream effector of AR. Inhibition of CaMKK2-AMPK signaling decreased GLUT12 translocation to the plasma membrane by inhibiting the phosphorylation of TBC1D4, a known regulator of glucose transport. Further, AR increasedTBC1D4expression. Correspondingly, expression ofTBC1D4correlated with AR activity in prostate cancer patient samples. Taken together, these data demonstrate that prostate cancer cells can increase the functional levels of GLUT12 through multiple mechanisms to promote glucose uptake and subsequent cell growth.

Prostate cancer cell growth inhibition by tamoxifen is associated with inhibition of protein kinase C and induction of p21waf1/cip1

The Prostate ◽  
1998 ◽  
Vol 37 (1) ◽  
pp. 51-59 ◽  
Author(s):  
Christian Rohlff ◽  
Mikhail V. Blagosklonny ◽  
Edward Kyle ◽  
Anuradha Kesari ◽  
Isaac Yi Kim ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Cell Growth ◽  
Growth Inhibition ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cell Growth Inhibition ◽  
Cancer Cell Growth ◽  
Kinase C
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