4.2 Article

gC1qR Expression in Normal and Pathologic Human Tissues: Differential Expression in Tissues of Epithelial and Mesenchymal Origin

Journal

JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY
Volume 60, Issue 6, Pages 467-474

Publisher

SAGE PUBLICATIONS LTD
DOI: 10.1369/0022155412440882

Keywords

gC1qR; immunohistochemistry; inflammation; neoplasia

Categories

Funding

  1. Division of Translational Laboratory Medicine of the Mount Sinai School of Medicine, New York, New York
  2. National Institute of Allergy and Infectious Diseases [R01-AI 060886, R01 AI-084178]

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The gC1qR (i.e., gC1q receptor, gC1q binding protein, p32, p33) is a multifunctional cellular protein that interacts with components of the complement, kinin, and coagulation cascades and select microbial pathogens. Enhanced gC1qR expression has been reported in adenocarcinomas arising in a variety of organs. The present study compared gC1qR expression in normal, inflammatory, dysplastic, and malignant tissue of epithelial and mesenchymal origin. gC1qR expression was visualized in tissue sections by immunohistochemistry using the 60.11 monoclonal antibody (i.e., IgG1 mouse monoclonal antibody directed against gC1qR) and the UltraVision LP Detection System. Sections were counterstained with hematoxylin and examined by light microscopy. Strongest gC1qR expression was noted in epithelial tumors of breast, prostate, liver, lung, and colon, as well as in squamous and basal cell carcinoma of the skin. However, increased gC1qR staining was appreciated also in inflammatory and proliferative lesions of the same cell types, as well as in normal continuously dividing cells. In contrast, tumors of mesenchymal origin generally stained weakly, with the exception of osteoblasts, which stained in both benign and malignant tissues. The data suggest that increased gC1qR expression may be a marker of benign and pathologic cell proliferation, particularly in cells of epithelial origin, with potential diagnostic and therapeutic applications. (J Histochem Cytochem 60:467-474, 2012)

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