期刊
EXPERT OPINION ON THERAPEUTIC TARGETS
卷 19, 期 5, 页码 617-632出版社
TAYLOR & FRANCIS LTD
DOI: 10.1517/14728222.2015.1005603
关键词
5 '-AMP-activated protein kinase; calcium/calmodulin-dependent protein kinase kinase 2; cancer metabolism; prostate cancer
资金
- Department of Medicine, Dresden
- Helmholtz Alliance ICEMED (Imaging and Curing Environmental Metabolic Diseases) through Initiative and Networking Fund of the Helmholtz Association
- DoD/PCRP [W81XWH-12-1-0204]
- Golfers Against Cancer
- Medical Research Service of the Veterans Affairs Department
- Department of Pathology
- Department of Medicine
- Division of Hematology/Oncology
- Sylvester Comprehensive Cancer Center
- University of Miami
- Miller School of Medicine
- South Florida Veterans Affairs Foundation for Research and Education
- Urology Care Foundation Research Scholars Program
- American Urological Association (AUA) Southeastern Section
Introduction: Increasing evidence suggests that prostate cancer cells undergo unique metabolic reprogramming during transformation. A master regulator of cellular homeostasis, 5'-AMP-activated protein kinase (AMPK), directs metabolic adaptation that supports the growth demands of rapidly dividing cancer cells. The utilization of AMPK as a therapeutic target may therefore provide an effective strategy in the treatment of prostate cancer. Areas covered: Our review describes the regulation of AMPK by androgens and upstream kinases including the calcium/calmodulin-dependent protein kinase kinase 2 (CaMKK2) in prostate cancer. Oncogenic, AMPK-regulated pathways that direct various metabolic processes are also addressed. Furthermore, we discuss the role of AMPK in growth arrest and autophagy as a potential survival pathway for cancer cells. In addition, by regulating non-metabolic pathways, AMPK may stimulate migration and mitosis. Finally, this review summarizes efforts to treat prostate cancer with pharmacological agents capable of modulating AMPK signaling. Expert opinion: Current research is primarily focused on developing drugs that activate AMPK as a treatment for prostate cancer. However, oncogenic aspects of AMPK signaling calls for caution about employing such therapies. We think that inhibitors of CaMKK2 or AMPK, or perhaps the modulation of downstream targets of AMPK, will gain importance in the clinical management of prostate cancer.
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