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Reciprocal cross-talk between Prostaglandin E2 and bone in prostate cancer: a current review.

Di Francesco S, Castellan P, Manco R, Tenaglia RL - Cent European J Urol (2011)

Bottom Line: Published studies were identified by searching computerized bibliographic systems from January 1(st), 2000 to July 1(st), 2011.An inversely low level of PGE2 exerts a stimulatory effect on osteoblastogenesis via activation of the Wnt pathway.Our finding suggests that PGE2 acts as a regulator in maintaining normal bone mass and indicate a mechanism whereby chemical manipulation of PGE2 levels or signaling may be therapeutically beneficial for prostate cancer treatment.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine and Aging Science, Section of Clinical Urology, ''G. D'Annunzio'' University, Chieti, Italy.

ABSTRACT
In this review we analyzed the role of PGE2 as a possible regulator of bone metabolism and bone metastases in prostate cancer. Published studies were identified by searching computerized bibliographic systems from January 1(st), 2000 to July 1(st), 2011. PGE2 represents a key factor in the modulation of bone metabolism and bone metastatic disease in prostate cancer interacting with bone regulatory signals including the RANK/RANKL/OPG system and Wnt pathways. A high concentration of PGE2 exerts a prevalent stimulatory effect on osteoclastogenesis via OPG/RANK/RANKL axis activation and a inhibitory effect on osteoblastogenesis trough inhibition of Wnt pathway. An inversely low level of PGE2 exerts a stimulatory effect on osteoblastogenesis via activation of the Wnt pathway. Our finding suggests that PGE2 acts as a regulator in maintaining normal bone mass and indicate a mechanism whereby chemical manipulation of PGE2 levels or signaling may be therapeutically beneficial for prostate cancer treatment.

No MeSH data available.


Related in: MedlinePlus

A schematic representation of aberrant expression of PGE2 in prostate cancer resulting in metabolic bone diseases. High-dose of PGE2 increased expression of Dkk-1 and sFRP, two potent Wnt inhibitors, predominants in osteolytic phase of Pca bone metastases. In more advanced osteoblastic phase of prostate cancer bone metastases, low dose of PGE2 can promote osteoblastogenesis activating Wnt pathway.
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Figure 0002: A schematic representation of aberrant expression of PGE2 in prostate cancer resulting in metabolic bone diseases. High-dose of PGE2 increased expression of Dkk-1 and sFRP, two potent Wnt inhibitors, predominants in osteolytic phase of Pca bone metastases. In more advanced osteoblastic phase of prostate cancer bone metastases, low dose of PGE2 can promote osteoblastogenesis activating Wnt pathway.

Mentions: The aberrant expression of PGE2, affect multiple pathways of bone formation and remodeling in prostate cancer. Imbalances in the bone remodeling process result in metabolic bone diseases characterized either by increased bone resorption (osteolytic bone metastases) or increased osteoblastic bone formation (prostate cancer-induced osteoblastic metastases) [20] (Fig. 2). PGE2 induces both increased osteoclastogenesis and osteoblastogenesis and can promote bone formation and resorption with catabolic or anabolic function [45, 47]. Continuous PGE2 administration stimulate bone catabolism while intermittent exposure led to bone anabolism as the result of imbalance in bone gain over loss with stimulation of endosteal bone formation [48].


Reciprocal cross-talk between Prostaglandin E2 and bone in prostate cancer: a current review.

Di Francesco S, Castellan P, Manco R, Tenaglia RL - Cent European J Urol (2011)

A schematic representation of aberrant expression of PGE2 in prostate cancer resulting in metabolic bone diseases. High-dose of PGE2 increased expression of Dkk-1 and sFRP, two potent Wnt inhibitors, predominants in osteolytic phase of Pca bone metastases. In more advanced osteoblastic phase of prostate cancer bone metastases, low dose of PGE2 can promote osteoblastogenesis activating Wnt pathway.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3921745&req=5

Figure 0002: A schematic representation of aberrant expression of PGE2 in prostate cancer resulting in metabolic bone diseases. High-dose of PGE2 increased expression of Dkk-1 and sFRP, two potent Wnt inhibitors, predominants in osteolytic phase of Pca bone metastases. In more advanced osteoblastic phase of prostate cancer bone metastases, low dose of PGE2 can promote osteoblastogenesis activating Wnt pathway.
Mentions: The aberrant expression of PGE2, affect multiple pathways of bone formation and remodeling in prostate cancer. Imbalances in the bone remodeling process result in metabolic bone diseases characterized either by increased bone resorption (osteolytic bone metastases) or increased osteoblastic bone formation (prostate cancer-induced osteoblastic metastases) [20] (Fig. 2). PGE2 induces both increased osteoclastogenesis and osteoblastogenesis and can promote bone formation and resorption with catabolic or anabolic function [45, 47]. Continuous PGE2 administration stimulate bone catabolism while intermittent exposure led to bone anabolism as the result of imbalance in bone gain over loss with stimulation of endosteal bone formation [48].

Bottom Line: Published studies were identified by searching computerized bibliographic systems from January 1(st), 2000 to July 1(st), 2011.An inversely low level of PGE2 exerts a stimulatory effect on osteoblastogenesis via activation of the Wnt pathway.Our finding suggests that PGE2 acts as a regulator in maintaining normal bone mass and indicate a mechanism whereby chemical manipulation of PGE2 levels or signaling may be therapeutically beneficial for prostate cancer treatment.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine and Aging Science, Section of Clinical Urology, ''G. D'Annunzio'' University, Chieti, Italy.

ABSTRACT
In this review we analyzed the role of PGE2 as a possible regulator of bone metabolism and bone metastases in prostate cancer. Published studies were identified by searching computerized bibliographic systems from January 1(st), 2000 to July 1(st), 2011. PGE2 represents a key factor in the modulation of bone metabolism and bone metastatic disease in prostate cancer interacting with bone regulatory signals including the RANK/RANKL/OPG system and Wnt pathways. A high concentration of PGE2 exerts a prevalent stimulatory effect on osteoclastogenesis via OPG/RANK/RANKL axis activation and a inhibitory effect on osteoblastogenesis trough inhibition of Wnt pathway. An inversely low level of PGE2 exerts a stimulatory effect on osteoblastogenesis via activation of the Wnt pathway. Our finding suggests that PGE2 acts as a regulator in maintaining normal bone mass and indicate a mechanism whereby chemical manipulation of PGE2 levels or signaling may be therapeutically beneficial for prostate cancer treatment.

No MeSH data available.


Related in: MedlinePlus