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Synthesis and Secretion of Plasminogen Activators and Plasminogen Activator Inhibitors in Cell Lines of Different Groups of Human Lung Tumors¹

Department of Internal Medicine, Division of Hematology/Oncology, Philipps University Marburg, 3550 Marburg [H-H. H., C. E., K. H.]; Center for Molecular Biology, 6900 Heidelberg [M. H., E. J.]; and German Cancer Research Center, 6900 Heidelberg [R. S-A.], Federal Republic of Germany

Several human lung tumor cell lines derived from large cell, squamous cell, and small cell carcinomas, as well as from mesotheliomas of the lung have been investigated for their gene expression and secretion of urokinase-type plasminogen activator (u-PA), tissue-type plasminogen activator (t-PA), and plasminogen activator inhibitors 1 and 2. All bronchogenic non-small cell carcinoma-derived cell lines studied could produce either plasminogen activators, their inhibitors, or both components, whereas in small cell lung carcinoma cell lines and cell lines derived from mesothelioma of the lung, no substantial amounts of any of these substances were synthesized. In detail, a large cell carcinoma-derived cell line, LCLC 97TM1, constitutively secreted large amounts of plasminogen activator. Northern blot analysis revealed RNA specific for u-PA and t-PA. Another large cell carcinoma-derived cell line, LCLC 103H, secreted smaller amounts of plasminogen activator and, additionally, plasminogen activator inhibitor. Specific mRNAs for u-PA and plasminogen activator inhibitors 1 and 2 were found in this cell line. In contrast, squamous cell carcinoma-derived cell lines secreted plasminogen activator only after treatment with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate; enhanced levels of u-PA, t-PA, and plasminogen activator inhibitor 1 mRNAs could then be demonstrated.

The different expression of the plasminogen activator enzyme system distinguishes cell lines derived of non-small cell lung carcinoma from those of small cell lung carcinoma and may also reflect significant differences in the biological behavior of these tumor types.

¹ This work was in part supported by the SFB 215 of the German Research Community and by the ZMBH (E. J.).

² To whom requests for reprints should be addressed, at the Institute of Immunology and Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, D-6900 Heidelberg, Federal Republic of Germany.

Received 11/29/88. Revised 7/19/89. Accepted 9/12/89.