ArticleCell death discovery2021
Mdivi-1 induces spindle abnormalities and augments taxol cytotoxicity in MDA-MB-231 cells.
Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 31 citations in OpenAlex.
- Mdivi-1 augments chlorpromazine's anticancer effect via modulation of mitochondrial dynamics, hallmarks of cancer-related cellular behavior, and oxidative stress.Medical oncology (Northwood, London, England) · 2026Article
- Super homotypic targeting by surface engineering of extracellular vesicles.Nature biomedical engineering · 2026Article
- Pioglitazone Ameliorates Mitochondrial Oxidative Stress and Inflammation via AMPK-Dependent Inhibition of Mitochondrial Fission in Leigh Syndrome.Cell proliferation · 2026Article
- The multifaceted roles of mitochondria and their therapeutic transformation: a new perspective on triple-negative breast cancer treatment.Frontiers in oncology · 2026Article
- Inhibitors of phosphodiesterase 1 enhance paclitaxel cytotoxicity in a MDA-MB-231-derived cell line by promoting microtubule stabilization.BBA advances · 2026Article
- Mitochondria and tumorigenesis: Molecular basis and therapeutic implications.Genes & diseases · 2026Review
- Vinpocetine Overcomes Paclitaxel Resistance in a Triple-Negative Breast Cancer Cell Line.Cell biology international · 2025Article
- Mitochondrial metabolism and cancer therapeutic innovation.Signal transduction and targeted therapy · 2025Review
- Drp1 knockdown aggravates obesity-induced cardiac dysfunction and remodeling.Mitochondrion · 2025Article
- Targeting Drp1 inhibits ESCC progression via the ROS-PGC1-α-Nrf1/2 pathway.Journal of translational medicine · 2025Article
- Exploiting Paradoxical Activation of Oncogenic MAPK Signaling by Targeting Mitochondria to SensitizeInternational journal of molecular sciences · 2025Article
- Thiostrepton induces spindle abnormalities and enhances Taxol cytotoxicity in MDA-MB-231 cells.Molecular biology reports · 2024Article
- NPRL2 is required for proliferation of oncogenic Ras-transformed bronchial epithelial cells.Cell division · 2024Article
- Mitochondrial division inhibitor (mdivi-1) induces extracellular matrix (ECM)-detachment of viable breast cancer cells by a DRP1-independent mechanism.Scientific reports · 2024Article
- Mitochondrial fission enhances IL-6-induced metastatic potential in ovarian cancer via ERK1/2 activation.Cancer science · 2024Article
- Prognostic value and immune regulatory role of dynamin 1-like in lung adenocarcinoma.Translational lung cancer research · 2023Article
- Inhibition of Drp1 orchestrates the responsiveness of breast cancer cells to paclitaxel but insignificantly relieves paclitaxel-related ovarian damage in mice.Scientific reports · 2023Article
- Spatial and temporal dynamics of ATP synthase from mitochondria toward the cell surface.Communications biology · 2023Article
- Mitochondrial Dynamin-Related Protein Drp1: a New Player in Cardio-oncology.Current oncology reports · 2022Review
- DRP1 contributes to head and neck cancer progression and induces glycolysis through modulated FOXM1/MMP12 axis.Molecular oncology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Taxol is a first-line chemotherapeutic for numerous cancers, including the highly refractory triple-negative breast cancer (TNBC). However, it is often associated with toxic side effects and chemoresistance in breast cancer patients, which greatly limits the clinical utility of the drug. Hence, compounds that act in concert with taxol to promote cytotoxicity may be useful to improve the efficacy of taxol-based chemotherapy. In this study, we demonstrated that mdivi-1, a putative inhibitor of mitochondrial fission protein Drp1, enhances the anticancer effects of taxol and overcomes taxol resistance in a TNBC cell line (MDA-MB-231). Not only did mdivi-1 induce mitotic spindle abnormalities and mitotic arrest when used alone, but it also enhanced taxol-induced antimitotic effects when applied in combination. In addition, mdivi-1 induced pronounced spindle abnormalities and cytotoxicity in a taxol-resistant cell line, indicating that it can overcome taxol resistance. Notably, the antimitotic effects of mdivi-1 were not accompanied by prominent morphological or functional alterations in mitochondria and were Drp1-independent. Instead, mdivi-1 exhibited affinity to tubulin at μM level, inhibited tubulin polymerization, and immediately disrupted spindle assembly when cells entered mitosis. Together, our results show that mdivi-1 associates with tubulin and impedes tubulin polymerization, actions which may underlie its antimitotic activity and its ability to enhance taxol cytotoxicity and overcome taxol resistance in MDA-MB-231 cells. Furthermore, our data imply a possibility that mdivi-1 could be useful to improve the therapeutic efficacy of taxol in breast cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.