6-ketoprostaglandin-f1-alpha and Prostatic-Neoplasms

The PC-3 Low Invasive cells and the PC-3 High Invasive cells were used to investigate the correlation of the COX-2 expression and its arachidonic acid metabolites, prostaglandins, with their invasiveness through Matrigel using a Boyden chamber assay. The COX-2 expression in PC-3 High Invasive cells was approximately 3-fold higher than in PC-3 Low Invasive cells while the COX-1 expression was similar in both cell sublines. When incubated with arachidonic acid, PGE2 was the major prostaglandin produced by these cells. PC-3 High Invasive cells produced PGE2 approximately 2.5-fold higher than PC-3 Low Invasive cells. PGD2 was the second most abundant prostaglandin produced by these cells. Both indomethacin (a nonspecific COX inhibitor) and NS-398 (a specific COX-2 inhibitor) inhibited the production of prostaglandins and the cell invasion. PGE2 alone did not induce the cell invasion of PC-3 Low Invasive cells. However, PGE2 reversed the inhibition of cell invasion by NS-398 and enhanced the cell invasion of the PC-3 High Invasive cells. In contrast, PGD2 slightly inhibited the cell invasion. These results suggest that in the PC-3 Low Invasive cells, COX-2-derived PGE2 may not be sufficient to induce cell invasion while in the PC-3 High Invasive cells, PGE2 may be sufficient to act as an enhancer for the cell invasion. Further, PGD2 may represent a weak inhibitor and counteracts the effect of PGE2 in the cell invasion.

Topics: 6-Ketoprostaglandin F1 alpha; Adenocarcinoma; Arachidonic Acid; Cyclooxygenase 1; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Dinoprost; Dinoprostone; Humans; Indomethacin; Isoenzymes; Male; Membrane Proteins; Neoplasm Invasiveness; Nitrobenzenes; Prostaglandin D2; Prostaglandin-Endoperoxide Synthases; Prostaglandins; Prostatic Neoplasms; Sulfonamides; Tumor Cells, Cultured

The discriminative ability of several skeletal and tumour markers was assessed in 102 patients with prostatic disease. These comprised serum acid and alkaline phosphatase, serum albumin and osteocalcin, urinary excretion of calcium, hydroxyproline and 6-oxo prostaglandin F1 alpha. None of the tests was of value in distinguishing patients with benign prostatic disease from those with tumour not involving the skeleton. Values of serum osteocalcin, urinary excretion of calcium and urinary 6-oxo prostaglandin F1 alpha failed to discriminate significantly between patients with or without metastases. The remaining four markers were compared by decision matrix analysis and receiver operating characteristic (ROC) curves. Serum alkaline phosphatase provided the most sensitive marker of skeletal metastases (80.5%), followed by serum acid phosphatase (80%), hydroxyproline (68%) and albumin (30%). ROC analysis suggested that alkaline phosphatase conformed most closely to the "ideal marker" with highest specificity and sensitivity.

Topics: 6-Ketoprostaglandin F1 alpha; Bone and Bones; Bone Neoplasms; Calcium; Calcium-Binding Proteins; Humans; Hydroxyproline; Male; Osteocalcin; Phosphoric Monoester Hydrolases; Prostatic Neoplasms; Serum Albumin

Topics: 6-Ketoprostaglandin F1 alpha; Clinical Laboratory Techniques; Diagnosis, Differential; Gas Chromatography-Mass Spectrometry; Humans; Male; Neoplasm Metastasis; Prognosis; Prostatic Hyperplasia; Prostatic Neoplasms; Reference Values