Malignant Epithelial Cells in Primary Human Lung Carcinomas Coexpress in vivo Platelet-Derived Growth Factor (PDGF) and PDGF Receptor mRNAs and Their Protein Products

• Published in: Proceedings of the National Academy of Sciences - PNAS 1992-05, Vol.89 (9), p.3942-3946
• Main Authors: Antoniades, Harry N., Galanopoulos, Theofanis, Neville-Golden, Janine, O'Hara, Carl J.
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Blood; Cancer; Carcinoma - genetics; Carcinoma - metabolism; Cellular biology; Connective tissue cells; Epithelial cells; Epithelium - physiopathology; Gene Expression; Humans; Idiopathic pulmonary fibrosis; Large cell carcinoma; Lung neoplasms; Lung Neoplasms - genetics; Lung Neoplasms - metabolism; Lungs; Medical research; Medical sciences; Messenger RNA; Nucleic Acid Hybridization; Platelet-Derived Growth Factor - genetics; Platelet-Derived Growth Factor - metabolism; Pneumology; Proteins; Proto-Oncogenes; Pulmonary Fibrosis - genetics; Pulmonary Fibrosis - metabolism; Receptors; Receptors, Cell Surface - genetics; Receptors, Cell Surface - metabolism; Receptors, Platelet-Derived Growth Factor; Ribonucleic acid; RNA; RNA, Messenger - genetics; Small cell lung carcinoma; Specimens; Tumors of the respiratory system and mediastinum
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.89.9.3942

Lung cancer represents one of the major human carcinomas with the highest degree of mortality. Epidemiologic studies have linked this disease to "chronic injury," largely induced by cigarette smoking. In the present studies, we demonstrate the in vivo expression of platelet-derived growth factor (PDGF) and PDGF receptor (PDGF-R) β mRNAs and their respective protein products in malignant epithelial cells of primary human lung carcinomas. In contrast, nonmalignant epithelial cells in control, normal lung tissue specimen did not express PDGF and PDGF-R mRNAs and did not produce their respective protein products. Epithelial cells in lung specimen from patients with idiopathic pulmonary fibrosis expressed only PDGF mRNA but not PDGF-R β mRNA. These findings of the inappropriate coexpression of a potent mitogen, PDGF, and its receptor in lung cancer epithelial cells suggest the presence of a powerful in vivo mechanism contributing to the self-stimulation and unregulated growth of lung cancer tumor cells.