中文摘要：

S100A9，钙绑定蛋白质，参予各种各样的肿瘤的煽动性的进程和开发，因此在癌症的领域里吸引许多注意生物学。这研究试图在 APL 调查 S100A9 和它的功能参与的规章的机制。我们使用了即时量的 PCR 决定 PML/RAR 是否在 ATRA 治疗之上在 NB4 和 PR9 房间影响 S100A9 的表示。基于薄片的 PCR 和双酶的记者试金系统被用来检测 PML/RAR 和 PU.1 怎么调整 S100A9 倡导者活动。当 S100A9 是 overexpressed 时， CCK-8 试金和流动 cytometry 被采用观察 NB4 房间的生存能力和 apoptosis。结果证明 S100A9 是 ATRA 应答的基因，并且 PML/RAR 为在 APL 房间的 S100A9 的导致 ATRA 的表示是必要的。另外， PU.1 能绑在 S100A9 的倡导者，特别当在 NB4 房间与 ATRA 对待时，并且支持它的活动。更重要地， S100A9 的 overexpression 导致了 NB4 房间的 apoptosis 并且禁止了房间生长。一起，我们的数据显示了那 PML/RAR， PU.1 为在 APL 房间的 S100A9 的导致 ATRA 的表达式是必要的。而且， S100A9 在 APL 房间支持了 apoptosis 并且影响了房间生长。

英文摘要：

S100A9, a calcium-binding protein, participates in the inflammatory process and development of various tumors, thus attracting much attention in the field of cancer biology. This study aimed to investigate the regulatory mechanism of SIOOA9 and its function involvement in APL. We used real-time quantitative PCR to determine whether PML/RARα affects the expression of S100A9 in NB4 and PR9 cells upon ATRA treatment. ChiP-based PCR and dual-luciferase reporter assay system were used to detect how PML/RARα and PU.1 regulate S100A9 promoter activity. CCK-8 assay and flow cytometry were employed to observe the viability and apoptosis of NB4 cells when S100A9 was overexpressed. Results showed that SIOOA9 was an ATRA-responsive gene, and PML/RARa was necessary for the ATRA-induced expression of SlOOA9 in APL cells. In addition, PU.1 could bind to the promoter of S100A9, especially when treated with ATRA in NB4 cells, and promote its activity. More importantly, overexpression of S100A9 induced the apoptosis of NB4 cells and inhibited cell growth. Collectively, our data indicated that PML/RARα and PU.1 were necessary for the ATRA-induced expression of S100A9 in APL cells. Furthermore, S100A9 promoted apoptosis in APL cells and affected cell growth.