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In vitro therapeutic effects of abemaciclib on triple-negative breast cancer cells
Zeynep Ozman1, Gamze Guney Eskiler2, Mehmet R Sekeroglu3
1Department of Medical Biochemistry, Faculty of Medicine, Bezmialem Vakif University, Istanbul, Turkey.
Abstract:
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.
Insights
Abemaciclib induces significant apoptotic cell death in triple-negative breast cancer (TNBC) by arresting cells and altering key protein levels. This suggests abemaciclib as a potential effective treatment for TNBC, though further research is needed.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Cyclin-dependent kinases 4 and 6 (CDK4/6) inhibitors have improved hormone-receptor-positive breast cancer treatment.
- The efficacy of abemaciclib in triple-negative breast cancer (TNBC) remains largely uncharacterized.
Purpose of the Study:
- To investigate the antiproliferative effects and cell death mechanisms of abemaciclib in TNBC cell lines (MDA-MB-231, MDA-MB-468) and a normal cell line (MCF-10A).
Main Methods:
- Annexin V staining, cell cycle analysis, caspase-3 activity assay, RT-PCR, acridine orange, DAPI staining.
- Autophagy assessment using autophagy-LC3 assay and acidic vesicular organelles staining.
Main Results:
- Abemaciclib induced significant apoptotic cell death in TNBC cells, characterized by G0/G1 cell cycle arrest and chromatin condensation.
- Key molecular changes included upregulation of caspase-3 and Bax, and downregulation of Bcl-2.
- Cytoplasmic vacuole formation was observed but not linked to autophagy.
Conclusions:
- Abemaciclib demonstrates potent antiproliferative and pro-apoptotic effects in TNBC cells.
- Abemaciclib represents a potential therapeutic strategy for TNBC.
- Further investigation is required to fully elucidate the mechanisms of abemaciclib-induced apoptosis and atypical cell death in TNBC.
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