Background: We previously detected that deltaNp63, a human p53 homologue, is an oncogene amplified in squamous cell carcinomas (SCC) including esophageal SCC. Subsequently, we examined global patterns of gene expression in cancer cells following deltaNp63 gene introduction using an oligonucleotide microarray approach. We identified S100A2, a Ca2+-binding protein, as a novel downstream mediator of deltaNp63.
Materials and methods: In this study, we examined S100A2 expression in esophageal SCC cell lines and primary SCCs using Northern analysis.
Results: We found that 2 out of 8 (25%) cell lines and 14 out of 30 primary esophageal cancers (47%) showed S100A2 gene overexpression compared to paired normal tissues. To examine a possible relationship between S100A2 overexpression and clinicopathological features, we proceeded with statistical analysis. S100A2 overexpression was significantly-associated with higher age in esophageal SCC (p=0.0434). Interestingly, S100A2-overexpressing cancers showed a trend toward preferentially developing lymph node metastases and distant metastases (p=0.111 and 0.178, respectively).
Conclusion: These results suggested that S100A2 might be related to the progression of esophageal SCC.