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Significance of Integrin 5 Gene Expression as a Prognostic Factor in Node-negative Non-Small Cell Lung Cancer¹

Department of Thoracic Surgery and Department V of Oncology, Kitano Hospital, Tazuke Kofukai Medical Research Institute, Kita-ku, Osaka 530-8480 [M. A., T. T., M. M.]; Department of Surgery, The Center for Adult Diseases of Osaka, Osaka 537-0025 [M. H.]; Second Department of Internal Medicine, Ehime University School of Medicine, Ehime 791-0295 [N. K.]; and First Department of Surgery, Kinki University School of Medicine, Osaka 589-8511 [H. I.], Japan

The integrin family plays a major role in complex biological events such as differentiation, development, wound healing, and the altered adhesive and invasive properties of tumor cells. Integrin 5ß1 is a classical fibronectin receptor, and it has been known as a tumor suppressor gene because tumor cells overexpressing 5ß1 are less tumorigenic than their parent cells. However, this finding conflicts with some recent data that suggests that the emergence of 5ß1 expression correlates with the tumor progression. We, therefore, investigated the expression of 5ß1 integrin in 20 lung cancer cell lines by flow cytometric analysis and in 88 node-negative non-small cell lung cancers (NSCLCs) by RT-PCR and immunohistochemical assays to determine the significance of this prognostic factor. In the 20 lung cancer cell lines, 8 (40.0%) cell lines strongly expressed integrin 5, 3 (15.0%) cell lines had moderate or weak 5 expression, and the remaining 9 (45.0%) cell lines expressed no integrin 5. In the 88 node-negative NSCLC patients, 44 samples (50.0%) were evaluated as having integrin 5 overexpression, and the integrin 5 expression was significantly associated with the status of differentiation and the age of the patients (P = 0.0379 and 0.0312, respectively). In the node-negative patients, the overall survival rate for patients with integrin 5 overexpressed tumors was significantly worse than for those individuals whose tumors had normal integrin 5 expression (P = 0.016).

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