The Clinical 
Significance of Plasma Urokinase-type Plasminogen Activator and Plasminogen Activator Inhibitor
Type 1 in Lung Cancer

Keimyung Medical Journal 2000;19(2):215-224.

The Clinical Significance of Plasma Urokinase-type Plasminogen Activator and Plasminogen Activator Inhibitor Type 1 in Lung Cancer

폐암 환자에서 Urokinase Type Plasminogen Activator 및 Plasminogen Activator Inhibitor Type 1의 임상적 의의

권순대; 최원일; 한승범; 권건영; 전영준

Abstract

Cancer invasion and metastasis require the dissolution of extracellular matrix in which sever?al proteolytic enzyme are involved. One of these enzyme the urokinase-type plasminogen acti-vator^-PA); and plasminogen activator inhibitor type l(PAI-l) have a possible role in cancer invasion and metastasis by protection of cancer itself from proteolysis by u-PA. It has been reported that the level of u-PA and PAI-1 in various cancer tissues are significantly higher than those in normal tissue and significant correlation with tumor size and lymph node involve?ment. We measured the concentration of plasma u-PA and PAI-1 antigens in patients with lung cancer and compared the concentration of them with histologic types and staging parameters; and also compared those concentrations in pre-treatment and post-treatment. In this study we measured the concentration of plasma u-PA and PAI-1 antigens using com?mercial ELISA kit in 40 lung cancer patients and 22 patient with benign lung diseases. The concentration of u-PA was 1.37 ±0.7 ng/mL in a group of benign lung disease patients and 1.75 ±0.75 ng/mL in lung cancer patients. The concentration of PAI-1 was 20.86 ± 13.2 ng/mL in benign lung disease and 20.09 ng/mL in lung cancer. The concentration of u-PA in lung can?cer patients was higher than those of benign lung disease patients. The concentration of u-PA was 2.42 ±2.69 ng/mL in lung cancer patients who were not treated; 1.78 ng±0.79 ng/mL in patients who were treated. The concentration of PAI-1 was 19.53 ±11.75 ng/mL in not-treated lung cancer patients; 10.71 ±6.26 ng/mL in treated patient group. The concentration of PAI-1 in treated lung cancer patients was lower than those of not-treated lung cancer patients. The concentration of u-PA was 1.82 ng/mL in stage I & II; 1.93 ±0.11 ng/mL in stage III; 1.65 ± 0.17 ng/mL in stage IV. The concentration of PAI-1 was 15.92 ±5.57 ng/mL in stage I & II; 20.95 ±0.54 ng/mL in stage III; 23.99±2.5 ng/mL in stage IV. The concentration of u-PA was 1.28 ±0.45 ng/mL in small cell carcinoma; 1.86 ±0.12 ng/mL in nonsmall cell carcinoma 1.76 ±0.0 ng/mL in squamous cell carcinoma 1.93 ±0.2 ng/mi in adenocarcinoma. The concentra?tion of PAI-1 was 18.74 ±3.83 ng/mL in small cell carcinoma 23.13 ±3.95 ng/mL in non- small cell carcinoma 25.39±2.81 ng/mL in squamous cell carcinoma 20.96±1.62 ng/mL in adenocarcinoma The plasma levels of u-PA in lung cancer patients were higher than those benign lung disease and plasma level of PAI-1 in who were treated (surgery; chemotherapy and/or radiotherapy) were lower than those who were not treated. These findings suggest involvement of U-PA with local invasion of lung cancer and possible roles in predicting the prognosis and survival of lung cancer patients.

Key Words: u-PA, PAI-2, Lung cancer