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Aim:To determine the effect of saposin C (a known trophic domain of prosaposin) on proliferation,migration andinvasion,as well as its effect on the expression of urokinase plasmonogen activator (uPA),its receptor (uPAR) andmatrix metalloproteinases (MMP)-2 and -9 in normal and malignant prostate cells.In addition,we tested whethersaposin C can activate p42/44 and stress-activated protein kinase/c-Jun NH_2-terminal kinase (SAPK/JNK) signaltransduction pathways of the mitogen-activated protein kinase (MAPK) superfamily.Methods:We employed West-ern blot analysis,phospho-specific antibodies,cell proliferation assay,reverse transcriptase-polymerase chain reaction,in vitro kinase assays and migration and invasion to determine the effect of saposin C on various biological behaviorsof prostate stromal and cancer cells.Results:Saposin C,in a cell type-specific manner,upregulates uPA/uPAR andimmediate early gene c-Jun expression,stimulates cell proliferation,migration and invasion and activates p42/44 andSAPK/JNK MAPK pathways in prostate stromal and cancer cells.Normal prostate epithelial cells were not responsiveto saposin C treatment in the above studies.Conclusion:Saposin C functions as a multipotential modulator of diversebiological activities in prostate cancer and stromal cells.These results strongly suggest that saposin C functions as apotent growth factor for prostatic cells and may contribute to prostate carcinogenesis and/or the development ofhormone-refractory prostate cancer.
Aim: To determine the effect of saposin C (a known trophic domain of prosaposin) on proliferation, migration and invasion, as well as its effect on the expression of urokinase plasmonogen activator (uPA), its receptor (uPAR) and matrix metalloproteinases (MMP) 2 and -9 in normal and malignant prostate cells. In addition, we tested whethersaposin C can activate p42 / 44 and stress-activated protein kinase / c-Jun NH_2-terminal kinase (SAPK / JNK) signaltransduction pathways of the mitogen-activated protein kinase (MAPK) superfamily. Methods: We employed West-ern blot analysis, phospho-specific antibodies, cell proliferation assay, reverse transcriptase-polymerase chain reaction, in vitro kinase assays and migration and invasion to determine the effect of saposin C on various biological behaviorsof prostate stromal and cancer cells. Results: Saposin C, in a cell type-specific manner, upregulates uPA / uPAR and immature early gene c-Jun expression, stimulates cell proliferation, migration and invasion and activates p42 / 44 andSAPK / JNK MAPK pathways in prostate stromal and cancer cells. Normal prostate epithelial cells were not responsive to saposin C treatment in the above studies. Confluence: Saposin C functions as a multipotential modulator of diverse biological activities in prostate cancer and stromal cells. results strongly suggest that saposin C functions as apotent growth factor for prostatic cells and may contribute to prostate carcinogenesis and / or the development ofhormone-refractory prostate cancer.