Department of Chemistry, National Tsing Hua University, Hsinchu 30013, Taiwan.
Graduate Institute of Biomedical Sciences and Center for Molecular Medicine, China Medical University, Taichung 40402, Taiwan.
Biomolecules. 2021 Apr 24;11(5):634. doi: 10.3390/biom11050634.
S100P, a small calcium-binding protein, associates with the p53 protein with micromolar affinity. It has been hypothesized that the oncogenic function of S100P may involve binding-induced inactivation of p53. We used H-N HSQC experiments and molecular modeling to study the molecular interactions between S100P and p53 in the presence and absence of pentamidine. Our experimental analysis indicates that the S100P-53 complex formation is successfully disrupted by pentamidine, since S100P shares the same binding site for p53 and pentamidine. In addition, we showed that pentamidine treatment of ZR-75-1 breast cancer cells resulted in reduced proliferation and increased p53 and p21 protein levels, indicating that pentamidine is an effective antagonist that interferes with the S100P-p53 interaction, leading to re-activation of the p53-21 pathway and inhibition of cancer cell proliferation. Collectively, our findings suggest that blocking the association between S100P and p53 by pentamidine will prevent cancer progression and, therefore, provide a new avenue for cancer therapy by targeting the S100P-p53 interaction.
S100P 是一种小的钙结合蛋白,以毫摩尔亲和力与 p53 蛋白结合。有人假设 S100P 的致癌功能可能涉及结合诱导的 p53 失活。我们使用 H-N HSQC 实验和分子建模来研究在存在和不存在戊二脒的情况下 S100P 和 p53 之间的分子相互作用。我们的实验分析表明,戊二脒成功地破坏了 S100P-53 复合物的形成,因为 S100P 与 p53 和戊二脒共享相同的结合位点。此外,我们表明,戊二脒处理 ZR-75-1 乳腺癌细胞导致增殖减少和 p53 和 p21 蛋白水平增加,表明戊二脒是一种有效的拮抗剂,可干扰 S100P-p53 相互作用,导致 p53-21 途径重新激活并抑制癌细胞增殖。总之,我们的研究结果表明,通过戊二脒阻断 S100P 和 p53 之间的关联将阻止癌症进展,因此通过靶向 S100P-p53 相互作用为癌症治疗提供了新途径。