The cyclin-dependent kinases 4 and 6 have led to a significant improvement in the treatment of hormone-receptor-positive breast cancer. However, the therapeutic potential of abemaciclib in triple-negative breast cancer (TNBC) has not been definitively elucidated. Therefore, the objective of this study was to investigate abemaciclib mediated antiproliferative effects on MDA-MB-231 and MDA-MB-468 TNBC and MCF-10A cell line through annexin V, cell cycle, caspase-3, reverse transcription-polymerase chain reaction analysis, acridine orange, and DAPI staining, for the first time. In addition, the autophagy-related cell death was assessed by autophagy-LC3 assay and acidic vesicular organelles staining. Our findings demonstrated that abemaciclib treatment resulted in significant apoptotic cell death in TNBC cells via G0/G1 arrest, chromatin condensation, the upregulation of caspase-3 and Bax levels, and the downregulation of Bcl-2. However, the formation of a large number of cytoplasmic vacuoles was not associated with autophagy. Therefore, abemaciclib treatment could be an effective treatment for TNBC. However, further studies are needed to elucidate the molecular mechanism of abemaciclib-induced apoptotic as well as atypical cell death derived from lysosomes in TNBC.

中文翻译：

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abemaciclib对三阴性乳腺癌细胞的体外治疗作用

细胞周期蛋白依赖性激酶 4 和 6 显着改善了激素受体阳性乳腺癌的治疗。然而，abemaciclib 在三阴性乳腺癌 (TNBC) 中的治疗潜力尚未明确阐明。因此，本研究的目的是通过膜联蛋白 V、细胞周期、caspase-3、逆转录聚合酶链反应研究 abemaciclib 介导的对 MDA-MB-231 和 MDA-MB-468 TNBC 和 MCF-10A 细胞系的抗增殖作用分析、吖啶橙和 DAPI 染色，这是第一次。此外，通过自噬-LC3测定和酸性囊泡细胞器染色评估自噬相关的细胞死亡。我们的研究结果表明，abemaciclib 治疗通过 G0/G1 期阻滞、染色质凝聚、Bax水平和Bcl-2的下调。然而，大量细胞质液泡的形成与自噬无关。因此，abemaciclib 治疗可能是 TNBC 的有效治疗方法。然而，需要进一步的研究来阐明 abemaciclib 诱导的 TNBC 溶酶体细胞凋亡和非典型细胞死亡的分子机制。