School of Pharmacy, College of Medicine, National Taiwan University, No. 1, Section 1, Jen-Ai Road, Taipei 100, Taiwan.
Biochem Pharmacol. 2012 Jul 1;84(1):59-67. doi: 10.1016/j.bcp.2012.03.023. Epub 2012 Apr 2.
Combination therapy, which can optimize killing activity to cancers and minimize drug resistance, is a mainstream therapy against hormone-refractory prostate cancers (HRPCs). Rottlerin, a natural polyphenolic component, synergistically increased PC-3 (a HRPC cell line) apoptosis induced by camptothecin (a topoisomerase I inhibitor). Using siRNA technique to knockdown protein kinase C-δ (PKCδ), the data showed that rottlerin-mediated synergistic effect was PKCδ-independent, although rottlerin has been used as a PKCδ inhibitor. Rottlerin potentiated camptothecin-induced DNA fragmentation at S phase and ATM phosphorylation at Ser1981. The effect was correlated to apoptosis (r2 = 0.9). To detect upstream signals, the data showed that camptothecin acted on and stabilized topoisomerase I-DNA complex, leading to the formation of camptothecin-trapped cleavage complexes (TOP1cc). The effect was potentiated by rottlerin. To determine DNA repair capability, the time-related γH2A.X formation was examined after camptothecin removal. Consequently, rottlerin significantly inhibited camptothecin removal-mediated decline of γH2A.X formation at S phase, indicating the impairment of DNA repair activity in the presence of rottlerin. The combinatory treatment of camptothecin and rottlerin induced conformational change and activation of Bax and formation of truncated Bad, suggesting the contribution of mitochondria stress to apoptosis. In summary, the data suggest that rottlerin-mediated camptothecin sensitization is through the augmented stabilization of TOP1cc, leading to an increase of DNA damage stress and, possibly, an impairment of DNA repair capability. Subsequently, mitochondria-involved apoptosis is triggered through Bax activation and truncated Bad formation. The novel discovery may provide an anticancer approach of combinatory use between rottlerin and camptothecin for the treatment of HRPCs.
联合治疗可以优化对癌症的杀伤活性,最小化耐药性,是治疗激素难治性前列腺癌(HRPC)的主流方法。罗特林是一种天然多酚成分,与喜树碱(拓扑异构酶 I 抑制剂)协同增加 PC-3(HRPC 细胞系)细胞凋亡。使用 siRNA 技术敲低蛋白激酶 C-δ(PKCδ),数据表明,罗特林介导的协同作用与 PKCδ 无关,尽管罗特林已被用作 PKCδ 抑制剂。罗特林增强了喜树碱诱导的 S 期 DNA 片段化和 ATM 磷酸化 Ser1981。这种作用与细胞凋亡相关(r2 = 0.9)。为了检测上游信号,数据表明,喜树碱作用于并稳定拓扑异构酶 I-DNA 复合物,导致喜树碱捕获的断裂复合物(TOP1cc)的形成。罗特林增强了这种作用。为了确定 DNA 修复能力,检查了喜树碱去除后与时间相关的 γH2A.X 形成。结果表明,罗特林显著抑制了 S 期喜树碱去除介导的 γH2A.X 形成的下降,表明在存在罗特林的情况下 DNA 修复活性受损。喜树碱和罗特林联合治疗诱导了 Bax 的构象变化和激活以及截断的 Bad 的形成,提示线粒体应激对细胞凋亡的贡献。总之,数据表明,罗特林介导的喜树碱增敏作用是通过 TOP1cc 的稳定性增强,导致 DNA 损伤应激增加,并且可能损害 DNA 修复能力。随后,通过 Bax 激活和截断的 Bad 形成触发线粒体参与的细胞凋亡。这一新发现可能为治疗 HRPC 提供一种联合使用罗特林和喜树碱的抗癌方法。