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ATR 和 WEE1 的联合抑制作为三阴性乳腺癌的一种新的治疗策略。

Combined Inhibition of ATR and WEE1 as a Novel Therapeutic Strategy in Triple-Negative Breast Cancer.

机构信息

Department of Medical Oncology, Jinling Hospital, Medical School of Nanjing University, Nanjing, China.

Department of Medical Oncology, Jinling Hospital, Medical School of Nanjing Medical University, Nanjing, China.

出版信息

Neoplasia. 2018 May;20(5):478-488. doi: 10.1016/j.neo.2018.03.003. Epub 2018 Mar 30.

Abstract

Triple negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer that poses a clinical challenge. Thus, new therapy strategies are urgently needed. The selective WEE1 inhibitor, AZD1775, has shown strong anti-proliferative effects on a variety of tumors. Here, we first demonstrate that inhibition of ATR by selective inhibitor AZD6738 can enhance AZD1775-caused growth inhibition in TNBC. Our results show that the enhanced cell death is attributed to repressed DNA damage repair and excessive replication stress, thereby causing increased DNA damage reflected by accumulation of the DNA double-strand-break marker γH2AX. On the other hand, combined treatment with AZD6738 and AZD1775 forces mitotic entry of cells with DNA damages by activating CDK1 activity, inducing severely aberrant mitosis and mitotic catastrophe, ultimately resulting in cell death. Dual inhibition of WEE1 and ATR also inactivated RAD51-mediated homologous recombination, which sensitized TNBC cells to cisplatin and PARP inhibitor. Here, based on the preclinical results that ATR inhibition synergizes with WEE1 inhibition in TNBC, we propose that this combination therapy alone, or in parallel with chemotherapy, represents an innovative and potent targeted therapy in TNBC.

摘要

三阴性乳腺癌(TNBC)是一种侵袭性很强的乳腺癌亚型,给临床治疗带来了挑战。因此,迫切需要新的治疗策略。选择性 WEE1 抑制剂 AZD1775 对多种肿瘤显示出很强的抗增殖作用。在这里,我们首次证明,ATR 的选择性抑制剂 AZD6738 的抑制作用可以增强 AZD1775 引起的 TNBC 生长抑制。我们的结果表明,抑制 DNA 损伤修复和过度复制应激引起的细胞死亡增加,导致 DNA 双链断裂标记 γH2AX 的积累增加,从而反映出 DNA 损伤的增加。另一方面,AZD6738 和 AZD1775 的联合治疗通过激活 CDK1 活性促使有 DNA 损伤的细胞进入有丝分裂,诱导严重异常有丝分裂和有丝分裂灾难,最终导致细胞死亡。ATR 和 WEE1 的双重抑制也抑制了 RAD51 介导的同源重组,使 TNBC 细胞对顺铂和 PARP 抑制剂敏感。在这里,基于 ATR 抑制与 TNBC 中的 WEE1 抑制协同作用的临床前结果,我们提出这种联合治疗单独或与化疗联合使用,代表了 TNBC 的一种创新和有效的靶向治疗方法。

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