ArticleCell cycle (Georgetown, Tex.)2020
The microtubule targeting agents eribulin and paclitaxel activate similar signaling pathways and induce cell death predominantly in a caspase-independent manner.
Article in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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14 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Comparative efficacy and safety of eribulin versus paclitaxel in breast cancer: a systematic review and meta-analysis.Future oncology (London, England) · 2024Pooled it
- Chemotherapy-Induced Alopecia in Breast Cancer Patients: Treatment-Specific Incidence and Risk of Persistent Hair Loss.Cancers · 2026Review
- Quinalizarin induces autophagy, apoptosis and mitotic catastrophe in cervical and prostate cancer cells.Scientific reports · 2025Article
- Immunomodulatory Effects of Halichondrin Isolated from Marine Sponges and Its Synthetic Analogs in Oncological Applications.Marine drugs · 2024Review
- Effects of Eribulin on the RNA Content of Extracellular Vesicles Released by Metastatic Breast Cancer Cells.Cells · 2024Article
- BCL-XL regulates the timing of mitotic apoptosis independently of BCL2 and MCL1 compensation.Cell death & disease · 2024Article
- E3 Ubiquitin LigaseCancers · 2023Article
- Phytochemicals as Chemo-Preventive Agents and Signaling Molecule Modulators: Current Role in Cancer Therapeutics and Inflammation.International journal of molecular sciences · 2022Review
- Sabizabulin, a Potent Orally Bioavailable Colchicine Binding Site Agent, Suppresses HER2+ Breast Cancer and Metastasis.Cancers · 2022Article
- A Mini Review on Molecules Inducing Caspase-Independent Cell Death: A New Route to Cancer Therapy.Molecules (Basel, Switzerland) · 2022Review
- Translocon-associated Protein Subunit SSR3 Determines and Predicts Susceptibility to Paclitaxel in Breast Cancer and Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- B Lymphocytes Are a Predictive Marker of Eribulin Response and Overall Survival in Locally Advanced or Metastatic Breast Cancer: A Multicenter, Two-Cohort, Non-Randomized, Open-Label, Retrospective Study.Frontiers in oncology · 2022Article
- Bcl-xL activity influences outcome of the mitotic arrest.Frontiers in pharmacology · 2022Article
- Methods for Chromosome Doubling.Methods in molecular biology (Clifton, N.J.) · 2021Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microtubule-targeting agents (MTAs) are the most effective chemotherapeutics used in cancer therapy to date, but their clinical use is often hampered by the acquisition of resistance. Thereby, elucidation of the molecular signaling pathways activated by novel FDA-approved MTAs such as eribulin is important for future therapeutic applications. In contrast to several reports, we show here that regardless of the presence of caspase-3, clinically relevant concentrations of eribulin and the classical MTA paclitaxel predominantly induce caspase-independent cell death in MCF-7 breast carcinoma cells. On the molecular level, several key proteins involved in apoptosis such as p53, Plk1, caspase-2, and Bim as well as the two MAPKs ERK and JNK were activated by both compounds to a similar extent. However, none of them proved to be important for eribulin- and paclitaxel-induced cytotoxicity, as their siRNA-mediated knockdown or inactivation by small molecule inhibitors did not alter cell death rates. In contrast, knockdown of the anti-apoptotic Bcl-2 protein, which becomes heavily phosphorylated at Ser70 during MTA treatment, resulted surprisingly in a reduction of MTA-mediated cell death. This phenomenon can be most likely explained by our observation that the absence of Bcl-2 slowed down cell cycle progression resulting in fewer cells entering mitosis, thereby delaying the mitotic capability of these MTAs to induce cell death. Taken together, although eribulin and paclitaxel disturb the mitotic spindle differently, they exhibit no functional differences in downstream molecular cell death signaling in MCF-7 breast cancer cells.
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