Limits...
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 bone metabolism regulation orchestrated by PGE2 concentration. High levels of PGE2 stimulate osteoclast differentiation through inhibition of OPG secretion, induction of RANKL expression in osteoblasts and stimulation of RANK expression in osteoclasts. Low levels of PGE2 results in defective osteoblast secretion of RANKL and impaired osteoclast formation, stimulation of preosteoblast cell growth, differentiation and Wnt signaling.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC3921745&req=5

Figure 0001: A schematic representation of bone metabolism regulation orchestrated by PGE2 concentration. High levels of PGE2 stimulate osteoclast differentiation through inhibition of OPG secretion, induction of RANKL expression in osteoblasts and stimulation of RANK expression in osteoclasts. Low levels of PGE2 results in defective osteoblast secretion of RANKL and impaired osteoclast formation, stimulation of preosteoblast cell growth, differentiation and Wnt signaling.

Mentions: PGE2 plays a critical role in bone remodeling and bone metastatic disease, stimulating osteoclast differentiation through inhibition of OPG secretion, induction of RANKL expression in osteoblasts, and stimulation of RANK expression in osteoclasts [20, 31–34]. PGE2 directly accelerate the physiological process of osteoclastogenesis and the development of large mature osteoclasts and indirectly regulate osteoclast numbers and morphology. Both stimulatory and inhibitory effects have been documented and the response may depend on the stage of development of the osteoclasts and on the prostaglandin receptors expressed [35] (Fig. 1). PGE2 initially exerts an inhibitory effect on RANKL activity and later a stimulatory effect on osteoclastogenesis (at doses > 1µM) via the OPG/RANK/RANKL system [33, 34]. Disruption of COX-2 gene expression and PGE2 results in defective osteoblast secretion of RANKL and impaired osteoclast formation, with more pronounced effects of PGE2 on osteoclasts when they were grown in coculture with osteoblasts [20, 36].


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 bone metabolism regulation orchestrated by PGE2 concentration. High levels of PGE2 stimulate osteoclast differentiation through inhibition of OPG secretion, induction of RANKL expression in osteoblasts and stimulation of RANK expression in osteoclasts. Low levels of PGE2 results in defective osteoblast secretion of RANKL and impaired osteoclast formation, stimulation of preosteoblast cell growth, differentiation and Wnt signaling.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 0001: A schematic representation of bone metabolism regulation orchestrated by PGE2 concentration. High levels of PGE2 stimulate osteoclast differentiation through inhibition of OPG secretion, induction of RANKL expression in osteoblasts and stimulation of RANK expression in osteoclasts. Low levels of PGE2 results in defective osteoblast secretion of RANKL and impaired osteoclast formation, stimulation of preosteoblast cell growth, differentiation and Wnt signaling.
Mentions: PGE2 plays a critical role in bone remodeling and bone metastatic disease, stimulating osteoclast differentiation through inhibition of OPG secretion, induction of RANKL expression in osteoblasts, and stimulation of RANK expression in osteoclasts [20, 31–34]. PGE2 directly accelerate the physiological process of osteoclastogenesis and the development of large mature osteoclasts and indirectly regulate osteoclast numbers and morphology. Both stimulatory and inhibitory effects have been documented and the response may depend on the stage of development of the osteoclasts and on the prostaglandin receptors expressed [35] (Fig. 1). PGE2 initially exerts an inhibitory effect on RANKL activity and later a stimulatory effect on osteoclastogenesis (at doses > 1µM) via the OPG/RANK/RANKL system [33, 34]. Disruption of COX-2 gene expression and PGE2 results in defective osteoblast secretion of RANKL and impaired osteoclast formation, with more pronounced effects of PGE2 on osteoclasts when they were grown in coculture with osteoblasts [20, 36].

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