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Updated: Sep 23, 2025
Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
Published on: March 20, 2020
Targeting Cell Death Mechanism Specifically in Triple Negative Breast Cancer Cell Lines
Lavinia-Lorena Pruteanu1,2,3, Cornelia Braicu4, Dezső Módos1
1Department of Chemistry, Centre for Molecular Science Informatics, University of Cambridge, Cambridge CB2 1EW, UK.
Abstract:
Triple negative breast cancer (TNBC) is currently associated with a lack of treatment options. Arsenic derivatives have shown antitumoral activity both in vitro and in vivo; however, their mode of action is not completely understood. In this work we evaluate the response to arsenate of the double positive MCF-7 breast cancer cell line as well as of two different TNBC cell lines, Hs578T and MDA-MB-231. Multimodal experiments were conducted to this end, using functional assays and microarrays. Arsenate was found to induce cytoskeletal alteration, autophagy and apoptosis in TNBC cells, and moderate effects in MCF-7 cells. Gene expression analysis showed that the TNBC cell lines' response to arsenate was more prominent in the G2M checkpoint, autophagy and apoptosis compared to the Human Mammary Epithelial Cells (HMEC) and MCF-7 cell lines. We confirmed the downregulation of anti-apoptotic genes (MCL1, BCL2, TGFβ1 and CCND1) by qRT-PCR, and on the protein level, for TGFβ2, by ELISA. Insight into the mode of action of arsenate in TNBC cell lines it is provided, and we concluded that TNBC and non-TNBC cell lines reacted differently to arsenate treatment in this particular experimental setup. We suggest the future research of arsenate as a treatment strategy against TNBC.
Insights
Arsenate shows promise as a treatment for triple-negative breast cancer (TNBC). This study found arsenate induces cell death and alters cell structure in TNBC cells more than in other breast cancer types.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Triple-negative breast cancer (TNBC) lacks targeted treatment options.
- Arsenic derivatives exhibit antitumoral effects, but their mechanisms are unclear.
Purpose of the Study:
- To investigate the response of TNBC cell lines (Hs578T, MDA-MB-231) and a non-TNBC cell line (MCF-7) to arsenate.
- To elucidate the mode of action of arsenate in different breast cancer subtypes.
Main Methods:
- Multimodal experiments including functional assays and microarrays.
- Quantitative real-time PCR (qRT-PCR) to confirm gene expression.
- Enzyme-linked immunosorbent assay (ELISA) for protein level analysis.
Main Results:
- Arsenate induced significant cytoskeletal alteration, autophagy, and apoptosis in TNBC cells.
- Gene expression analysis revealed a more prominent response in TNBC cells at the G2M checkpoint, autophagy, and apoptosis.
- Downregulation of anti-apoptotic genes (MCL1, BCL2, TGFβ1, CCND1) and TGFβ2 protein was confirmed.
Conclusions:
- TNBC and non-TNBC cell lines exhibit differential responses to arsenate treatment.
- Arsenate's mode of action involves inducing apoptosis and affecting cell cycle checkpoints in TNBC.
- Arsenate warrants further investigation as a potential therapeutic strategy for TNBC.
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