Kudryavtsev Vladimir A, Khokhlova Anna V, Mosina Vera A, Selivanova Elena I, Kabakov Alexander E
Department of Radiation Biochemistry, A. Tsyb Medical Radiological Research Center, Obninsk, Russia.
PLoS One. 2017 Mar 14;12(3):e0173640. doi: 10.1371/journal.pone.0173640. eCollection 2017.
We studied a role of the inducible heat shock protein 70 (Hsp70) in cellular response to radiosensitizing treatments with inhibitors of the heat shock protein 90 (Hsp90) chaperone activity. Cell lines derived from solid tumors of different origin were treated with the Hsp90 inhibitors (17AAG, geldanamycin, radicicol, NVP-AUY922) or/and γ-photon radiation. For comparison, human cells of the non-cancerous origin were subjected to the same treatments. We found that the Hsp90 inhibitors yielded considerable radiosensitization only when they cause early and pronounced Hsp70 induction; moreover, a magnitude of radiosensitization was positively correlated with the level of Hsp70 induction. The quantification of Hsp70 levels in Hsp90 inhibitor-treated normal and cancer cells enabled to predict which of them will be susceptible to any Hsp90-inhibiting radiosensitizer as well as what concentrations of the inhibitors ensure the preferential cytotoxicity in the irradiated tumors without aggravating radiation damage to adjacent normal tissues. Importantly, the Hsp70 induction in the Hsp90 inhibitor-treated cancer cells appears to be their protective response that alleviates the tumor-sensitizing effects of the Hsp90 inactivation. Combination of the Hsp70-inducing inhibitors of Hsp90 with known inhibitors of the Hsp induction such as quercetin, triptolide, KNK437, NZ28 prevented up-regulation of Hsp70 in the cancer cells thereby increasing their post-radiation apoptotic/necrotic death and decreasing their post-radiation viability/clonogenicity. Similarly, co-treatment with the two inhibitors conferred the enhanced radiosensitization of proliferating rather than quiescent human vascular endothelial cells which may be used for suppressing the tumor-stimulated angiogenesis. Thus, the easily immunodetectable Hsp70 induction can be a useful marker for predicting effects of Hsp90-inhibiting radiosensitizers on tumors and normal tissues exposed to ionizing radiation. Moreover, targeting the Hsp70 induction in Hsp90 inhibitor-treated cancer cells and tumor vasculature cells may beneficially enhance the radiosensitizing effect.
我们研究了诱导型热休克蛋白70(Hsp70)在细胞对热休克蛋白90(Hsp90)伴侣活性抑制剂的放射增敏治疗反应中的作用。用Hsp90抑制剂(17AAG、格尔德霉素、放线菌酮、NVP - AUY922)或/和γ光子辐射处理源自不同实体瘤的细胞系。作为对照,对源自非癌组织的人类细胞进行相同处理。我们发现,Hsp90抑制剂仅在引起早期且显著的Hsp70诱导时才产生显著的放射增敏作用;此外,放射增敏程度与Hsp70诱导水平呈正相关。对经Hsp90抑制剂处理的正常细胞和癌细胞中Hsp70水平的定量分析,能够预测哪些细胞对任何Hsp90抑制性放射增敏剂敏感,以及何种浓度的抑制剂能确保在不加重对相邻正常组织辐射损伤的情况下,优先对受照射肿瘤产生细胞毒性。重要的是,经Hsp90抑制剂处理的癌细胞中Hsp70的诱导似乎是一种保护反应,可减轻Hsp90失活对肿瘤的增敏作用。将诱导Hsp70的Hsp90抑制剂与已知的Hsp诱导抑制剂(如槲皮素、雷公藤内酯醇、KNK437、NZ28)联合使用,可防止癌细胞中Hsp70的上调,从而增加其辐射后凋亡/坏死死亡,并降低其辐射后活力/克隆形成能力。同样,两种抑制剂联合处理可增强增殖期而非静止期人类血管内皮细胞的放射增敏作用,这可能用于抑制肿瘤刺激的血管生成。因此,易于免疫检测的Hsp70诱导可作为一个有用的标志物,用于预测Hsp90抑制性放射增敏剂对暴露于电离辐射的肿瘤和正常组织的影响。此外,针对经Hsp90抑制剂处理的癌细胞和肿瘤脉管系统细胞中的Hsp70诱导进行靶向干预,可能有益地增强放射增敏效果。