Abstract:
:The aim of the study was to demonstrate the role of parathyroid hormone related protein (PTHrP) in stimulating aldo-keto reductase (AKR) 1C3 expression in prostate cancer (CaP) cells. CaP cell proliferation and resistance to apoptosis was increased by PTHrP transfection. Conversely, reducing AKR1C3 expression by siRNA decreased cell proliferation. Since these effects could be mediated through AKR1C3-catalyzed reductions of the PPARγ ligand, 15-DeoxyΔ(12,14)-PGJ(2), we treated the cells with prostaglandins (PG). (PG) D(2) inhibited cell proliferation, but its metabolite, 9α,11β-PGF(2), did not effect CaP cell growth. The AKR1C family members serve as potential therapeutic targets for CaP therapy.
journal_name
Cancer Lettjournal_title
Cancer lettersauthors
Downs TM,Burton DW,Araiza FL,Hastings RH,Deftos LJdoi
10.1016/j.canlet.2011.02.027subject
Has Abstractpub_date
2011-07-01 00:00:00pages
52-9issue
1eissn
0304-3835issn
1872-7980pii
S0304-3835(11)00120-0journal_volume
306pub_type
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