The SPARC protein: an overview of its role in lung cancer and pulmonary fibrosis and its potential role in chronic airways disease

The SPARC (secreted protein acidic and rich in cysteine) protein is matricellular molecule regulating interactions between cells and their surrounding extracellular matrix (ECM). This protein thus governs fundamental cellular functions such as cell adhesion, proliferation and differentiation. SPARC...

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Bibliographic Details
Published in:British journal of pharmacology 2017-01, Vol.174 (1), p.3-14
Main Authors: Wong, Sharon L I, Sukkar, Maria B
Format: Article
Language:English
Subjects:
Animals
Asthma
Chronic obstructive pulmonary disease
Humans
Lung cancer
Lung Neoplasms - metabolism
Osteonectin - metabolism
Proteins
Pulmonary Disease, Chronic Obstructive - metabolism
Pulmonary fibrosis
Pulmonary Fibrosis - metabolism
Review
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Summary:The SPARC (secreted protein acidic and rich in cysteine) protein is matricellular molecule regulating interactions between cells and their surrounding extracellular matrix (ECM). This protein thus governs fundamental cellular functions such as cell adhesion, proliferation and differentiation. SPARC also regulates the expression and activity of numerous growth factors and matrix metalloproteinases essential for ECM degradation and turnover. Studies in SPARC‐null mice have revealed a critical role for SPARC in tissue development, injury and repair and in the regulation of the immune response. In the lung, SPARC drives pathological responses in non‐small cell lung cancer and idiopathic pulmonary fibrosis by promoting microvascular remodelling and excessive deposition of ECM proteins. Remarkably, although chronic airway conditions such as asthma and chronic obstructive pulmonary disease (COPD) involve significant remodelling in both the airway and vascular compartments, the role of SPARC in these conditions has thus far been overlooked. In this review, we discuss the role of SPARC in lung cancer and pulmonary fibrosis, as well as potential mechanisms by which it may contribute to the disease process in asthma and COPD.
ISSN:0007-1188
1476-5381
DOI:10.1111/bph.13653