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Overexpression of JAM-A in non-small cell lung cancer correlates with tumor progression.

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.
AuthorsMin Zhang, Wenting Luo, Bo Huang, Zihui Liu, Limei Sun, Qingfu Zhang, Xueshan Qiu, Ke Xu, Enhua Wang
JournalPloS one (PLoS One) Vol. 8 Issue 11 Pg. e79173 ( 2013) ISSN: 1932-6203 [Electronic] United States
PMID24265754 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Cell Adhesion Molecules
  • F11R protein, human
  • Receptors, Cell Surface
Topics
  • Carcinoma, Non-Small-Cell Lung (genetics, pathology)
  • Cell Adhesion Molecules (deficiency, genetics)
  • Cell Line, Tumor
  • Cell Membrane (metabolism)
  • Cell Proliferation
  • Disease Progression
  • Female
  • G1 Phase Cell Cycle Checkpoints (genetics)
  • Gene Expression Regulation, Neoplastic
  • Gene Knockdown Techniques
  • Humans
  • Lung Neoplasms (genetics, pathology)
  • Male
  • Receptors, Cell Surface (deficiency, genetics)

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