Hibi Kenji, Fujitake Shin-ichi, Takase Tsunenobu, Kodera Yasuhiro, Ito Katsuki, Akiyama Seiji, Shirane Masatoshi, Nakao Akimasa
Gastroenterological Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8560, Japan.
Clin Cancer Res. 2003 Sep 15;9(11):4282-5.
It has been proved recently that DeltaNp63 may play an oncogenic role in the tumorigenic pathway of squamous cell cancers. To gain additional insight into this pathway, we examined global patterns of gene expression in cancer cells after DeltaNp63 gene introduction using the oligonucleotide microarray approach.
We found that S100A2 might be a target of the DeltaNp63 pathway. To confirm the data obtained from oligonucleotide microarray, we then examined the interaction of DeltaNp63 to S100A2. S100A2 induction was strictly dependent on DeltaNp63 expression by DeltaNp63 transgene and Northern analysis. DeltaNp63 transactivated the S100A2 promoter, and significantly more fold changes were seen in DeltaNp63-introduced cells than in p53-introduced cells, suggesting that DeltaNp63 may be a novel stimulator of the S100A2 promoter.
Taken together, this evidence would seem to suggest that S100A2 is a novel downstream mediator of DeltaNp63.
最近已证实，DeltaNp63可能在鳞状细胞癌的致瘤途径中发挥致癌作用。为了进一步深入了解该途径，我们使用寡核苷酸微阵列方法检测了导入DeltaNp63基因后癌细胞中的基因表达全局模式。
我们发现S100A2可能是DeltaNp63途径的一个靶点。为了证实从寡核苷酸微阵列获得的数据，我们随后检测了DeltaNp63与S100A2的相互作用。通过DeltaNp63转基因和Northern分析，S100A2的诱导严格依赖于DeltaNp63的表达。DeltaNp63可反式激活S100A2启动子，并且在导入DeltaNp63的细胞中观察到的倍数变化明显多于导入p53的细胞，这表明DeltaNp63可能是S100A2启动子的一种新型刺激因子。
综上所述，这些证据似乎表明S100A2是DeltaNp63的一种新型下游介质。
