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髓系细胞白血病1小分子抑制剂S63845与顺铂在三阴性乳腺癌中协同作用。

Myeloid Cell Leukemia 1 Small Molecule Inhibitor S63845 Synergizes with Cisplatin in Triple-Negative Breast Cancer.

作者信息

Acton Alexus, Placzek William J

机构信息

Department of Biochemistry and Molecular Genetics, University of Alabama at Birmingham (UAB), Birmingham, AL 35294, USA.

出版信息

Cancers (Basel). 2023 Sep 8;15(18):4481. doi: 10.3390/cancers15184481.

Abstract

Triple-negative breast cancer (TNBC) is an aggressive cancer that lacks specific molecular targets that are often used for therapy. The refractory rate of TNBC to broad-spectrum chemotherapy remains high; however, the combination of newly developed treatments with the current standard of care has delivered promising anti-tumor effects. One mechanism employed by TNBC to avoid cell death is the increased expression of the anti-apoptotic protein, myeloid cell leukemia 1 (MCL1). Multiple studies have demonstrated that increased MCL1 expression enables resistance to platinum-based chemotherapy. In addition to suppressing apoptosis, we recently demonstrated that MCL1 also binds and negatively regulates the transcriptional activity of TP73. TP73 upregulation is a critical driver of cisplatin-induced DNA damage response, and ultimately, cell death. We therefore sought to determine if the coadministration of an MCL1-targeted inhibitor with cisplatin could produce a synergistic response in TNBC. This study demonstrates that the MCL1 inhibitor, S63845, combined with cisplatin synergizes by inducing apoptosis while also decreasing proliferation in a subset of TNBC cell lines. The use of combined MCL1 inhibitors with cisplatin in TNBC effectively initiates TAp73 anti-tumor effects on cell cycle arrest and apoptosis. This observation provides a molecular profile that can be exploited to identify sensitive TNBCs.

摘要

三阴性乳腺癌(TNBC)是一种侵袭性癌症,缺乏常用于治疗的特定分子靶点。TNBC对广谱化疗的难治率仍然很高;然而,新开发的治疗方法与当前护理标准的结合已产生了有前景的抗肿瘤效果。TNBC避免细胞死亡所采用的一种机制是抗凋亡蛋白髓样细胞白血病1(MCL1)的表达增加。多项研究表明,MCL1表达增加会导致对铂类化疗产生耐药性。除了抑制细胞凋亡外,我们最近还证明MCL1还结合并负向调节TP73的转录活性。TP73上调是顺铂诱导的DNA损伤反应以及最终细胞死亡的关键驱动因素。因此,我们试图确定MCL1靶向抑制剂与顺铂联合使用是否能在TNBC中产生协同反应。这项研究表明,MCL1抑制剂S63845与顺铂联合使用时,通过诱导细胞凋亡以及减少一部分TNBC细胞系中的增殖发挥协同作用。在TNBC中使用MCL1抑制剂与顺铂联合,可有效启动TAp73对细胞周期阻滞和细胞凋亡的抗肿瘤作用。这一观察结果提供了一个可用于识别敏感TNBC的分子特征。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9bb8/10526511/3e927b289482/cancers-15-04481-g001.jpg

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