Expression of the focal adhesion protein paxillin in lung cancer and its relation to cell motility (original) (raw)

Oncogene volume 18, pages 67–77 (1999)Cite this article

Abstract

Lung cancer can lead to abnormalities of the actin cytoskeleton structure which may be important in transformation. In this study, we have investigated the expression of the cytoskeletal associated protein paxillin in lung cancer. Paxillin is a 68 kDa focal adhesion protein, with four tandem LIM domains at the C-terminus, involved in growth factor receptor, integrin and oncogenic signaling such as v-src, BCR/ABL, and E6 of the papilloma virus. In non-small cell lung cancer (NSCLC) cell lines, paxillin localized to the focal adhesions. The possible role of paxillin in lung cancer cells was assessed by overexpressing green fluorescence protein (GFP)-paxillin construct in two separate NSCLC cell lines (Calu-1 and H661). Over the course of 48 h, GFP-paxillin consistently caused the cells to become round and to decrease cell motility as compared to normal controls, GFP-N-terminus paxillin, or GFP-LIM transfected cells. Because some lung cancers may be quite aggressive and metastasize quickly, which may be related to the cytoskeleton, we determined the expression of paxillin in NSCLC and small cell lung cancer (SCLC) cell lines and patient tumor tissues. Expression of paxillin in NSCLC and SCLC cell lines were determined by Northern blot and Western blot analysis. The expression of paxillin was consistently low in SCLC cell lines, whereas there was paxillin expression in NSCLC cell lines. There was a variability of expression of paxillin in NSCLC tumor tissue as compared to normal lung tissue. In contrast, by immunohistochemistry, we show that there was no detectable expression of paxillin in 5/5 SCLC patients. This data suggests that absence or low level of paxillin protein expression may cause certain lung cancers, such as SCLC, to be more motile and possibly more aggressive.

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Acknowledgements

This work was partially supported by: Jose Carreras International Leukemia Foundation Fellowship FIJC-95/INT (to MS), NIH grants DK50654 (to JDG) and CA75348 (to RS).

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Authors and Affiliations

  1. Division of Hematologic Oncology, Dana-Farber Cancer Institute and Harvard Medical School, 44 Binney Street, Boston, 02115, Massachusetts, USA
    Ravi Salgia, Jian-Liang Li, Darren S Ewaniuk, Martin Sattler, Wen-Che Chen, Evan Pisick & James D Griffin
  2. Division of Cellular and Molecular Biology, Dana-Farber Cancer Institute and Harvard Medical School, 44 Binney Street, Boston, 02115, Massachusetts, USA
    You-Bin Wang & Lan Bo Chen
  3. Division of Neoplastic Disease Mechanisms, Dana-Farber Cancer Institute and Harvard Medical School, 44 Binney Street, Boston, 02115, Massachusetts, USA
    Geoffrey I Shapiro & Barrett J Rollins
  4. Division of Thoracic Oncology and Adult Oncology, Dana-Farber Cancer Institute and Harvard Medical School, 44 Binney Street, Boston, 02115, Massachusetts, USA
    Ravi Salgia, William Richards, Geoffrey I Shapiro, Barrett J Rollins & David J Sugarbaker

Authors

  1. Ravi Salgia
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  2. Jian-Liang Li
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  3. Darren S Ewaniuk
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  4. You-Bin Wang
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  5. Martin Sattler
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  6. Wen-Che Chen
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  7. William Richards
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  8. Evan Pisick
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  9. Geoffrey I Shapiro
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  10. Barrett J Rollins
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  11. Lan Bo Chen
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  12. James D Griffin
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  13. David J Sugarbaker
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Salgia, R., Li, JL., Ewaniuk, D. et al. Expression of the focal adhesion protein paxillin in lung cancer and its relation to cell motility.Oncogene 18, 67–77 (1999). https://doi.org/10.1038/sj.onc.1202273

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