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Article

Overexpression of type VI collagen in neoplastic lung tissues

  • Authors:
    • Larry Voiles
    • David E. Lewis
    • Ling Han
    • Ivan P. Lupov
    • Tsang-Long Lin
    • Michael J. Robertson
    • Irina Petrache
    • Hua-Chen Chang
  • View Affiliations / Copyright

    Affiliations: Department of Biology, Indiana University-Purdue University Indianapolis School of Science, Indianapolis, IN, USA, Department of Comparative Pathobiology, Animal Disease Diagnostic Laboratory, Purdue University College of Veterinary Medicine, West Lafayette, IN, USA, The Bone Marrow and Stem Cell Transplantation Program, Lymphoma Program and the Division of Hematology/Oncology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, USA, Division of Pulmonary, Allergy, Critical Care, Occupational and Sleep Medicine, Department of Medicine, Indiana University School of Medicine and the ̔Richard L. Roudebush’ VA Medical Center, Indianapolis, IN, USA
  • Pages: 1897-1904
    |
    Published online on: August 22, 2014
       https://doi.org/10.3892/or.2014.3438
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Abstract

Type VI collagen (COL6), an extracellular matrix protein, is important in maintaining the integrity of lung tissue. An increase in COL6 mRNA and protein deposition was found in the lungs of patients with pulmonary fibrosis, a chronic inflammatory condition with a strong association with lung cancer. In the present study, we demonstrated overexpression of COL6 in the lungs of non-small cell lung cancers. We hypothesized that excessive COL6 in the lung interstitium may exert stimulatory effects on the adjacent cells. In vitro stimulation of monocytes with COL6 resulted in the production of IL-23, which may promote tumor development in an environment of IL-23-mediated lung inflammation, where tissue modeling occurs concurrently with excessive COL6 production. In addition, COL6 was capable of stimulating signaling pathways that activate focal adhesion kinase and extracellular signal‑regulated kinase 1/2 in lung epithelial cells, which may also facilitate the development of lung neoplasms. Taken together, our data suggest the potential role of COL6 in promoting lung neoplasia in diseased lungs where COL6 is overexpressed.
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Copy and paste a formatted citation
Spandidos Publications style
Voiles L, Lewis DE, Han L, Lupov IP, Lin T, Robertson MJ, Petrache I and Chang H: Overexpression of type VI collagen in neoplastic lung tissues. Oncol Rep 32: 1897-1904, 2014.
APA
Voiles, L., Lewis, D.E., Han, L., Lupov, I.P., Lin, T., Robertson, M.J. ... Chang, H. (2014). Overexpression of type VI collagen in neoplastic lung tissues. Oncology Reports, 32, 1897-1904. https://doi.org/10.3892/or.2014.3438
MLA
Voiles, L., Lewis, D. E., Han, L., Lupov, I. P., Lin, T., Robertson, M. J., Petrache, I., Chang, H."Overexpression of type VI collagen in neoplastic lung tissues". Oncology Reports 32.5 (2014): 1897-1904.
Chicago
Voiles, L., Lewis, D. E., Han, L., Lupov, I. P., Lin, T., Robertson, M. J., Petrache, I., Chang, H."Overexpression of type VI collagen in neoplastic lung tissues". Oncology Reports 32, no. 5 (2014): 1897-1904. https://doi.org/10.3892/or.2014.3438
Copy and paste a formatted citation
x
Spandidos Publications style
Voiles L, Lewis DE, Han L, Lupov IP, Lin T, Robertson MJ, Petrache I and Chang H: Overexpression of type VI collagen in neoplastic lung tissues. Oncol Rep 32: 1897-1904, 2014.
APA
Voiles, L., Lewis, D.E., Han, L., Lupov, I.P., Lin, T., Robertson, M.J. ... Chang, H. (2014). Overexpression of type VI collagen in neoplastic lung tissues. Oncology Reports, 32, 1897-1904. https://doi.org/10.3892/or.2014.3438
MLA
Voiles, L., Lewis, D. E., Han, L., Lupov, I. P., Lin, T., Robertson, M. J., Petrache, I., Chang, H."Overexpression of type VI collagen in neoplastic lung tissues". Oncology Reports 32.5 (2014): 1897-1904.
Chicago
Voiles, L., Lewis, D. E., Han, L., Lupov, I. P., Lin, T., Robertson, M. J., Petrache, I., Chang, H."Overexpression of type VI collagen in neoplastic lung tissues". Oncology Reports 32, no. 5 (2014): 1897-1904. https://doi.org/10.3892/or.2014.3438
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