BACKGROUND: Activation of the plasminogen/plasmin system seems to contribute to tumor aggressiveness and shorter post-operative survival. In the present study we examined the relation of uPA (urokinase plasminogen activator), uPAR (uPA receptor) and PAI-1 (plasminogen activator inhibitor type 1) to the biological growth behavior of esophageal cancer, as well as their influence on survival in esophageal cancer. MATERIALS AND METHODS: The expression and distribution of uPA, uPAR and PAI-1 were analyzed by Northern blot analysis and immunostaining in 41 resected esophageal cancers and in normal esophagi. RESULTS: Northern blot analysis revealed a 5.0-, 3.6- and 5.4-fold increase in uPA, uPAR, and PAI-1 mRNA levels in esophageal cancer, respectively, in comparison to normal controls (p<0.01). These mRNA moieties were concomitantly increased in 86% of the tumors. uPA activity was 2.3-fold increased in esophageal cancer compared with normal controls (p<0.01). Statistical analysis revealed no differences in uPA, uPAR and PAI-1 immunoreactivity between well-differentiated, moderately-differentiated and poorly-differentiated tumors. Furthermore, survival analysis showed no difference in patients whose tumors exhibited positive uPA and uPAR immunostaining (median 11 months, range 4-36 months) versus patients whose tumors exhibited negative uPA and uPAR immunostaining (median 11 months, range 3-51 months). CONCLUSION: Our data revealed that overexpression of uPA, uPAR and PAI-1 is often present in human esophageal carcinomas. However, up-regulation of these factors is not correlated with tumor differentiation or survival. These findings indicate that, unlike other tumors, uPA, uPAR and PAI-1 seem not to be prognostic markers for esophageal carcinomas.
BACKGROUND: Activation of the plasminogen/plasmin system seems to contribute to tumor aggressiveness and shorter post-operative survival. In the present study we examined the relation of uPA (urokinase plasminogen activator), uPAR (uPA receptor) and PAI-1 (plasminogen activator inhibitor type 1) to the biological growth behavior of esophageal cancer, as well as their influence on survival in esophageal cancer. MATERIALS AND METHODS: The expression and distribution of uPA, uPAR and PAI-1 were analyzed by Northern blot analysis and immunostaining in 41 resected esophageal cancers and in normal esophagi. RESULTS: Northern blot analysis revealed a 5.0-, 3.6- and 5.4-fold increase in uPA, uPAR, and PAI-1 mRNA levels in esophageal cancer, respectively, in comparison to normal controls (p<0.01). These mRNA moieties were concomitantly increased in 86% of the tumors. uPA activity was 2.3-fold increased in esophageal cancer compared with normal controls (p<0.01). Statistical analysis revealed no differences in uPA, uPAR and PAI-1 immunoreactivity between well-differentiated, moderately-differentiated and poorly-differentiated tumors. Furthermore, survival analysis showed no difference in patients whose tumors exhibited positive uPA and uPAR immunostaining (median 11 months, range 4-36 months) versus patients whose tumors exhibited negative uPA and uPAR immunostaining (median 11 months, range 3-51 months). CONCLUSION: Our data revealed that overexpression of uPA, uPAR and PAI-1 is often present in humanesophageal carcinomas. However, up-regulation of these factors is not correlated with tumor differentiation or survival. These findings indicate that, unlike other tumors, uPA, uPAR and PAI-1 seem not to be prognostic markers for esophageal carcinomas.
Authors: Daniel Brungs; Julia Chen; Morteza Aghmesheh; Kara L Vine; Therese M Becker; Martin G Carolan; Marie Ranson Journal: Oncotarget Date: 2017-04-04