Significance of semaphorin-3A and MMP-14 protein expression in non-small cell lung cancer

Semaphorin-3A is a chemorepellent guidance protein that is crucial in regulating the tumor microenvironment. MMP-14, a membrane-anchored matrix metalloproteinase, is closely associated with extracellular matrix (ECM) remodeling and cell migration in the progression of cancer metastasis. In the present study, the correlation between the expression levels of semaphorin-3A and MMP-14, and their subsequent prognostic significance in non-small cell lung cancer (NSCLC), was investigated. The expression of semaphorin-3A and MMP-14 protein levels was analyzed in 94 cases of NSCLC tissues and in 80 cases of normal lung tissues, using immunohistochemistry (IHC). Correlation and survival analysis were used to further investigate their association and prognostic value. The results revealed that the NSCLC tissues exhibited a lower expression of semaphorin-3A and a higher expression of MMP-14 than in the control lung tissues. The downregulation of semaphorin-3A and upregulation of MMP-14 may promote pleural invasion, lymph node metastasis, vascular invasion and proliferating cell nuclear antigen expression. The expression of semaphorin-3A was correlated with the maximum diameter of tumor. There was a negative correlation between the protein expression levels of semaphorin-3A and MMP-14 in NSCLC tissues. Furthermore, we identified that the patients with lower expression of semaphorin-3A and a higher expression of MMP-14 had worse disease prognosis. The data suggest that lower expression of semaphorin-3A and a higher expression of MMP-14 may promote occurrence and development in NSCLC and that the combined detection of semaphorin-3A and MMP-14 protein may be a helpful tool in predicting the prognosis of NSCLC.

• Publication year

  2014

• Venue

  Oncology Letters

• Publication date

  2014-02-27

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.3892/ol.2014.1920PMID 24765144PMCID 3997704
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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