Tuberc Respir Dis > Volume 44(3); 1997 > Article
Tuberculosis and Respiratory Diseases 1997;44(3):516-524.
DOI: https://doi.org/10.4046/trd.1997.44.3.516    Published online June 1, 1997.
The Significance of Plasma Urokinase-type Plasminogen Activator and Type 1 Plasminogen Activator Inhibitor in Lung Cancer.
Won Young Lee, Kwang Joo Park, Hyung Jung Kim, Chul Min Ahn, Doo Yun Lee, Joon Chang, Sung Kyu Kim
Abstract
BACKGROUND
Cancer invasion and metastasis require the dissolution of the extracellular matrix in which several proteolytic enzymes are Involved. One of these enzymes is the urokinase - type plasminogen activator(u-PA), and plasminogen activator inhibitors(PAI-1, PAI-2) a]so 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 love]s of u-PA and plasminogen activator inhibitors in various cancer tissues are significantly higher than those in normal tissues and have significant correlations with tumor size and lymph node involvement Here, we measured the concentration of plasma u-PA and PAI- 1 antigens in the patients with lung cancer and compared the concentration of them with histologic types and staging parameters. METHODS: We measured the concentration of plasma u-PA and PAI-1 antigens using commercial ELISA kit in 37 lung cancer patients, 21 benign lung disease patients and 24 age-matched healthy controls, and we compared the concentration of them with histologic types and staging parameters in lung cancer patients. RESULTS: The concentration of u-PA was 1.0α0.3ng/mL in controls, 1.0α0.3ng/mL in benign lung disease patients and 0.9α0.3ng/mL in lung cancer patients. The concentration of PAI-1 was 14.2α6.7ng/mL in controls, 14.9α6.3ng/mL in benign lung disease patients, and 22.1 α9.8ng/mL in lung cancer patients. The concentration of PAI- 1 in lung cancer patients was higher than those of benign lung disease patients and controls. The concentration of u-PA was 0.7α0.4ng/mL in squamous cell carcinoma, 0.8α 0.3ng/mL in adenocarcinoma, 0.9ng/mL in large cell carcinoma, and 1.1α0.7ng/mL in small cell carcinoma. The concert traction of PAI-1 was 22.3α7.2ng/mL in squamous cell carcinoma, 22.6α9.9ng/mL in adenocarcinoma, 42ng/mL in large cell carcinoma, and 16.0α14.2ng/mL in small cell carcinoma. The concentration of u-PA was 0.74ng/mL in stage I, 1.2α0.6ng/mL in stage II, 0.7 α 0.4ng/mL in stage IIIA, 0.7α0.4ng/mL in stage IIIB, and 0.7α0.3ng/mL in stage IV. The concentration of PAI-1 was 21.8ng/mL in stage I, 22.7α8.7ng/mL in stage II, 18.4 α4.9ng/mL in stage IIIA, 25.3α9.0ng/mL in stage IIIB, and 21.5α10.8ng /mL in stage IV. When we divided T stage unto T1-3 and 74, the concentration of u-PA was 0.8α 0.4ng/mL in T1-3 and 0.7α0.4ng/mL in T4, and the concentration of PAI-1 was 17.9α 5.6ng/mL in T1-3 and 26.1α9.1ng/mL in T4. The concentration of PAI-1 in T4 was significantly higher than that in T1-3. The concentration of u-PA was 0.8α 0.4ng/mL in M0 and 0.7α0.3ng/mL in Ml, and the concentration of PAI-1 was 23.6α8.3ng/mL in M0 and 21.5α10.8ng/mL in M1 CONCLUSIONS: The plasma levels of PAI-1 in lung cancer were higher than benign lung disease and control, and the plasma levels of PAI-1 in 74 were significantly higher than T1-3. These findings suggest involvement of PAI-1 with local invasion of lung cancer, but it should be confirmed by the data on comparison with pathological staging and tissue level in lung cancer.
Key Words: Urokinase-type plasminogen activator, u-PA, Type 1 plasminogen activator inhibitor, PAI-1, Lung cancer


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