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 (uP...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 whether saposin C can activate p42/44 and stress-activated protein kinase/c-Jun NH_2-terminal kinase (SAPK/JNK) signal transduction 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 behaviors of prostate stromal and cancer cells.Results:Saposin C,in a cell type-specific manner,upregulates uPA/uPAR and immediate early gene c-Jun expression,stimulates cell proliferation,migration and invasion and activates p42/44 and SAPK/JNK MAPK pathways in prostate stromal and cancer cells.Normal prostate epithelial cells were not responsive to saposin C treatment in the above studies.Conclusion:Saposin C functions as a multipotential modulator of diverse biological activities in prostate cancer and stromal cells.These results strongly suggest that saposin C functions as a potent growth factor for prostatic cells and may contribute to prostate carcinogenesis and/or the development of hormone-refractory prostate cancer.展开更多
目的 探讨 u PA、u PAR基因表达和肝癌转移、肝细胞癌门静脉主干癌栓 (Tum or thrombosid of the m ain trunkof the portal vein,PVTT)形成的关系。方法 采用原位杂交等技术检测 u PA、u PAR表达。结果 癌栓 (A1组 )和其原发癌(A2组...目的 探讨 u PA、u PAR基因表达和肝癌转移、肝细胞癌门静脉主干癌栓 (Tum or thrombosid of the m ain trunkof the portal vein,PVTT)形成的关系。方法 采用原位杂交等技术检测 u PA、u PAR表达。结果 癌栓 (A1组 )和其原发癌(A2组 ) u PA、u PAR m RNA阳性表达率均高于无转移肝癌 (B组 ) (P均 <0 .0 1) ;A 1组表达强度均高于 A2组 (P<0 .0 1)。 A 2组小血管内可见癌细胞群落 ,A 1组多见 ,B组无此现象。 A1组、A 2组 u PAR和 u PA蛋白质阳性表达率均高于 B组 (P均 <0 .0 1) ,A1组表达强度均高于 A2组 (P<0 .0 1)。 u PA、u PAR m RNA和其蛋白质表达存在良好相关性 (P均 <0 .0 1)。结论 u PA、u PAR在肝癌的侵袭和转移中起重要作用 ,其过度表达是展开更多
文摘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 whether saposin C can activate p42/44 and stress-activated protein kinase/c-Jun NH_2-terminal kinase (SAPK/JNK) signal transduction 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 behaviors of prostate stromal and cancer cells.Results:Saposin C,in a cell type-specific manner,upregulates uPA/uPAR and immediate early gene c-Jun expression,stimulates cell proliferation,migration and invasion and activates p42/44 and SAPK/JNK MAPK pathways in prostate stromal and cancer cells.Normal prostate epithelial cells were not responsive to saposin C treatment in the above studies.Conclusion:Saposin C functions as a multipotential modulator of diverse biological activities in prostate cancer and stromal cells.These results strongly suggest that saposin C functions as a potent growth factor for prostatic cells and may contribute to prostate carcinogenesis and/or the development of hormone-refractory prostate cancer.
文摘目的 探讨 u PA、u PAR基因表达和肝癌转移、肝细胞癌门静脉主干癌栓 (Tum or thrombosid of the m ain trunkof the portal vein,PVTT)形成的关系。方法 采用原位杂交等技术检测 u PA、u PAR表达。结果 癌栓 (A1组 )和其原发癌(A2组 ) u PA、u PAR m RNA阳性表达率均高于无转移肝癌 (B组 ) (P均 <0 .0 1) ;A 1组表达强度均高于 A2组 (P<0 .0 1)。 A 2组小血管内可见癌细胞群落 ,A 1组多见 ,B组无此现象。 A1组、A 2组 u PAR和 u PA蛋白质阳性表达率均高于 B组 (P均 <0 .0 1) ,A1组表达强度均高于 A2组 (P<0 .0 1)。 u PA、u PAR m RNA和其蛋白质表达存在良好相关性 (P均 <0 .0 1)。结论 u PA、u PAR在肝癌的侵袭和转移中起重要作用 ,其过度表达是
