Activation of rapid signaling pathways does not contribute to 1α,25-dihydroxyvitamin D3-induced growth inhibition of mouse prostate epithelial progenitor cells
✍ Scribed by Jia Li; James C. Fleet; Dorothy Teegarden
- Publisher
- John Wiley and Sons
- Year
- 2009
- Tongue
- English
- Weight
- 146 KB
- Volume
- 107
- Category
- Article
- ISSN
- 0730-2312
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✦ Synopsis
Abstract
The active form of vitamin D, 1α,25‐dihydroxyvitamin D~3~ (1,25(OH)~2~D) inhibits the growth of prostate epithelial cells, however the underlying mechanisms have not been clearly delineated. In the current study, the impact of 1,25(OH)~2~D on the rapid activation of extracellular‐regulated kinase (ERK) 1/2 and protein kinase C α (PKCα), and the role of these pathways in growth inhibition was examined in immortalized mouse prostate epithelial cells, MPEC3, that exhibit stem/progenitor cell characteristics. 1,25(OH)~2~D treatment suppressed the growth of MPEC3 in a dose and time dependent manner (e.g., 21% reduction at three days with 100 nM 1,25(OH)~2~D treatment). However, ERK1/2 activity was not altered by 100 nM 1,25(OH)~2~D treatment for time points from 1 min to 1 h in either serum‐containing or serum‐free medium. Similarly, PKCα activation (translocation onto the plasma membrane) was not regulated by short‐term treatment of 100 nM 1,25(OH)~2~D. In conclusion, 1,25(OH)~2~D did not mediate rapid activation of ERK1/2 or PKCα in MPEC3 and therefore the growth inhibitory effect of 1,25(OH)~2~D is independent of rapid activation of these signaling pathways in this cell type. J. Cell. Biochem. 107: 1031–1036, 2009. © 2009 Wiley‐Liss, Inc.
This article was published online 2 June 2009. An error was subsequently identified. This notice is included in the online and print versions to indicate that both have been corrected 15 June 2009.