ArticleInternational journal of molecular sciences2023
MCL1 Inhibition Overcomes the Aggressiveness Features of Triple-Negative Breast Cancer MDA-MB-231 Cells.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- The combination of rosuvastatin and meloxicam enhances the radiotherapy efficacy of MCF7, T-47D, and MDA-MB-231 breast cancer cell lines.Research in pharmaceutical sciences · 2026Article
- Evaluating the Antiproliferative Effects of Tri(2-Furyl)- and Triphenylphosphine-Gold(I) Pyridyl- and Pyrimidine-Thiolate Complexes.Biomolecules · 2026Article
- The role of pluripotency regulators in triple-negative breast cancer immune response.Frontiers in genetics · 2026Review
- Crosstalk between miRNAs and oxidative stress: implications for cancer pathogenesis and therapy.Functional & integrative genomics · 2025Review
- Anoikis resistance in Cancer: Mechanisms, therapeutic strategies, potential targets, and models for enhanced understanding.Cancer letters · 2025Review
- Stemness of Cancer: A Study of Triple-negative Breast Cancer From a Neuroscience Perspective.Stem cell reviews and reports · 2025Review
- Extra Virgin Olive Oil Polyphenol-Enriched Extracts Exert Antioxidant and Anti-Inflammatory Effects on Peripheral Blood Mononuclear Cells from Rheumatoid Arthritis Patients.Antioxidants (Basel, Switzerland) · 2025Article
- Adipokines in Breast Cancer: Decoding Genetic and Proteomic Mechanisms Underlying Migration, Invasion, and Proliferation.Breast cancer (Dove Medical Press) · 2025Article
- Review
- Transcriptomics analysis identified ezrin as a potential druggable target in cervical and gastric cancer cells.Clinics (Sao Paulo, Brazil) · 2024Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Triple-Negative Breast Cancer (TNBC) is a particularly aggressive subtype among breast cancers (BCs), characterized by anoikis resistance, high invasiveness, and metastatic potential as well as Epithelial-Mesenchymal Transition (EMT) and stemness features. In the last few years, our research focused on the function of MCL1, an antiapoptotic protein frequently deregulated in TNBC. Here, we demonstrate that MCL1 inhibition by A-1210477, a specific BH3-mimetic, promotes anoikis/apoptosis in the MDA-MB-231 cell line, as shown via an increase in proapoptotic markers and caspase activation. Our evidence also shows A-1210477 effects on Focal Adhesions (FAs) impairing the integrin trim and survival signaling pathways, such as FAK, AKT, ERK, NF-κB, and GSK3β-inducing anoikis, thus suggesting a putative role of MCL1 in regulation of FA dynamics. Interestingly, in accordance with these results, we observed a reduction in migratory and invasiveness capabilities as confirmed by a decrease in metalloproteinases (MMPs) levels following A-1210477 treatment. Moreover, MCL1 inhibition promotes a reduction in EMT characteristics as demonstrated by the downregulation of Vimentin, MUC1, DNMT1, and a surprising re-expression of E-Cadherin, suggesting a possible mesenchymal-like phenotype reversion. In addition, we also observed the downregulation of stemness makers such as
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