Department of Pathology, Stony Brook Medicine, Stony Brook, New York, NY 11794, USA.
Cells. 2023 Dec 26;13(1):49. doi: 10.3390/cells13010049.
Chemoresistance and inefficient therapeutic efficacies in triple-negative breast cancers (TNBCs) are among the major clinical problems in breast cancers. A potential new method to sensitize these tumors to current treatment options is, therefore, urgent and necessary. Our previous studies demonstrated that miR-489 serves as one of the top tumor-suppressing miRs and features downregulated expression in metastatic TNBCs and that the restoration of miR-489 expression in TNBCs effectively inhibits the metastatic potentials of TNBCs both in vitro and in vivo. The chemical modification of miR-489 (CMM489) through the replacement of uracil with 5-FU further enhances the therapeutic potential of miR-489. In the present study, we tested the effects of CMM489 in synergizing DNA damage response (DDR) inhibitors such as PARP inhibitors. CMM489 is particularly effective in sensitizing TNBC cell lines with inherent resistance to PARP inhibitors regardless of BRCA mutation status. One of the anti-cancer mechanisms through which CMM489 synergizes with PARP inhibitors is the blockade of homologous recombination (HR) in TNBC cells upon DNA damage. The results of this study highlight the potential use of CMM489 in combination treatments with PARP inhibitors in TNBCs.
在三阴性乳腺癌(TNBC)中,化疗耐药性和低效的治疗效果是乳腺癌的主要临床问题之一。因此,迫切需要一种新的方法来使这些肿瘤对当前的治疗选择敏感。我们之前的研究表明,miR-489 作为一种顶级肿瘤抑制 miR 之一,在转移性 TNBC 中表达下调,并且在 TNBC 中恢复 miR-489 的表达可有效抑制 TNBC 的转移潜能,无论是在体外还是体内。通过用 5-FU 替换尿嘧啶对 miR-489 进行化学修饰(CMM489)进一步增强了 miR-489 的治疗潜力。在本研究中,我们测试了 CMM489 与 DNA 损伤反应(DDR)抑制剂(如 PARP 抑制剂)协同作用的效果。CMM489 特别有效地增强了对 PARP 抑制剂固有耐药性的 TNBC 细胞系的敏感性,而与 BRCA 突变状态无关。CMM489 与 PARP 抑制剂协同作用的抗癌机制之一是在 DNA 损伤时阻断 TNBC 细胞中的同源重组(HR)。这项研究的结果强调了 CMM489 与 PARP 抑制剂联合治疗 TNBC 的潜在用途。