Conclusions
Our results will provide the basis for more mechanistic studies on the role of COX-2 in PaCa and may help to develop novel therapeutic strategies aiming at the COX-2/prostanoid pathway.
Methods
Cyclooxygenase-2-negative MIA PaCa-2 cells were stably transduced with COX-2 or control viruses (MP2 and MP2). Prostaglandin E2 (PGE2) production was measured by liquid chromatography and tandem mass spectrometry. Anchorage-dependent and -independent cell growth was analyzed by cell count and 3-dimensional collagen cell culture system, respectively. Changes in apoptotic gene expression were measured by a polymerase chain reaction array. The growth of tumors in vivo was evaluated in a xenograft animal model.
Results
Stable expression of COX-2 increased anchorage-dependent and -independent cell growth, which was accompanied by elevated PGE2 production. Several significant differences in apoptotic gene expression were detected between MP2 and MP2 cells. Furthermore, MP2 cells grew faster than MP2 cells in a xenograft animal model. Conclusions: Our results will provide the basis for more mechanistic studies on the role of COX-2 in PaCa and may help to develop novel therapeutic strategies aiming at the COX-2/prostanoid pathway.