Abstract
The objective of the current study was to determine the clinical significance of junctional adhesion molecule A (JAM-A) in patients with non-small cell lung cancer (NSCLC) and the biological function of JAM-A in NSCLC cell lines. We showed that JAM-A is predominantly expressed in cell membranes and high expression of JAM-A occurred in 37% of lung tumor specimens compared to corresponding normal tissues. High expression of JAM-A was significantly correlated with TNM stage (P = 0.021), lymph node metastasis (P = 0.007), and decreased overall survival (P = 0.02), In addition, we observed that silencing JAM-A by small interfering RNA inhibited tumor cell proliferation and induced cell cycle arrest at the G1/S boundary. Western blotting analysis revealed that knockdown of JAM-A decreased the protein levels of cyclin D1, CDK4, 6, and P-Rb. Thus, JAM-A plays an important role in NSCLC progression.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Carcinoma, Non-Small-Cell Lung / genetics*
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Carcinoma, Non-Small-Cell Lung / pathology
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Cell Adhesion Molecules / deficiency
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Cell Adhesion Molecules / genetics*
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Cell Line, Tumor
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Cell Membrane / metabolism
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Cell Proliferation
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Disease Progression*
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Female
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G1 Phase Cell Cycle Checkpoints / genetics
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Gene Expression Regulation, Neoplastic*
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Gene Knockdown Techniques
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Humans
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Lung Neoplasms / genetics*
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Lung Neoplasms / pathology
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Male
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Receptors, Cell Surface / deficiency
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Receptors, Cell Surface / genetics*
Substances
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Cell Adhesion Molecules
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F11R protein, human
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Receptors, Cell Surface
Grants and funding
This work was supported by grants from National Natural Science Foundation of China (No. 30972967) and Research Fund for the Doctoral Program of the Higher Education of China (No. 20092104110018). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.