Abstract:
:AMP-activated protein kinase (AMPK) has recently emerged as a potential target for cancer therapy due to the observation that activation of AMPK inhibits tumor cell growth. It is well-known that androgen receptor (AR) signaling is a major driver for the development and progression of prostate cancer and that downregulation of AR is a critical step in the induction of apoptosis in prostate cancer cells. However, little is known about the potential interaction between AMPK and AR signaling pathways. In the current study, we showed that activation of AMPK by metformin caused decrease of AR protein level through suppression of AR mRNA expression and promotion of AR protein degradation, demonstrating that AMPK activation is upstream of AR downregulation. We also showed that inhibition of AR function by an anti-androgen or its siRNA enhanced AMPK activation and growth inhibition whereas overexpression of AR delayed AMPK activation and increased prostate cancer cellular resistance to metformin treatment, suggesting that AR suppresses AMPK signaling-mediated growth inhibition in a feedback mechanism. Our findings thus reveal a novel AMPK-AR regulatory loop in prostate cancer cells and should have a potential clinical significance.
journal_name
J Cell Physioljournal_title
Journal of cellular physiologyauthors
Shen M,Zhang Z,Ratnam M,Dou QPdoi
10.1002/jcp.24494subject
Has Abstractpub_date
2014-06-01 00:00:00pages
688-95issue
6eissn
0021-9541issn
1097-4652journal_volume
229pub_type
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journal_title:Journal of cellular physiology
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journal_title:Journal of cellular physiology
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