ArticleFrontiers in oncology2021
Wnt/β-Catenin Inhibition Disrupts Carboplatin Resistance in Isogenic Models of Triple-Negative Breast Cancer.
Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Keratin 6A Overexpression in the Lymphovascular Invasion-Associated Tumor Subgroup Promotes Progression of Triple-Negative Breast Cancer.Cancer research and treatment · 2026Article
- ZNF468 stabilization by RNF4 enhances apoptosis resistance and carboplatin resistance in breast cancer via transcription activation of XIAP.Genes & genomics · 2026Article
- Wnt signaling promotes inflammation and EMT-associated gene expression in mesenchymal TNBC.Scientific reports · 2026Article
- Eugenoplatin (a phyto-chemo drug conjugate) targets cancer stem cells through inhibition of the β-catenin signaling in triple-negative breast cancer cells.Journal of translational medicine · 2026Article
- Chemotherapy-Treated Breast Cancer Cells Activate the WNT Signaling Pathway to Enter a Diapause-Like Early Persister State.Cancer research · 2026Article
- The impact of the telomerase inhibitor on the Wnt signaling pathway in breast cancer and breast cancer stem cells.Molecular biology reports · 2026Article
- Wnt/β-Catenin-mTOR-autophagy crosstalk in breast cancer: context-dependent control of tumor progression, immune suppression, and therapeutic resistance.Frontiers in immunology · 2026Review
- PI3 K/AKT/mTOR pathway and its role in breast cancer stem cells.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- IL-3/STAT5/miR-155-5p axis supports stem-related pathway reprogramming in TNBC.Breast cancer research : BCR · 2025Article
- Overexpression of alcohol dehydrogenase 1 A inhibits the progress of triple negative breast cancer via Wnt/β-catenin signaling.Scientific reports · 2025Article
- An update on cancer stem cell survival pathways involved in chemoresistance in triple-negative breast cancer.Future oncology (London, England) · 2025Review
- Effect of siRNA-mediated LGR5 Inhibition on the Expression of Stemness-related Genes in Triple-negative Breast Cancer Spheroid Model.Advanced biomedical research · 2025Article
- Immunotherapy resistance in triple-negative breast cancer: Molecular mechanisms, tumor microenvironment, and therapeutic implications.Frontiers in oncology · 2025Review
- Role of EMT in drug resistance of breast cancer: molecular mechanisms and therapeutic strategies.Frontiers in oncology · 2025Review
- Blocking the WNT/β-catenin pathway in cancer treatment:pharmacological targets and drug therapeutic potential.Heliyon · 2024Review
- Breast Cancer Stem Cells and Tumor Heterogeneity: Characteristics and Therapeutic Strategies.Cancers · 2024Review
- A review of biological targets and therapeutic approaches in the management of triple-negative breast cancer.Journal of advanced research · 2023Review
- WNT-Conditioned Mechanism of Exit from Postchemotherapy Shock of Differentiated Tumour Cells.Cancers · 2023Article
- Signaling pathways governing the maintenance of breast cancer stem cells and their therapeutic implications.Frontiers in cell and developmental biology · 2023Review
- Challenges for Triple Negative Breast Cancer Treatment: Defeating Heterogeneity and Cancer Stemness.Cancers · 2022Review
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-Negative Breast Cancer (TNBC) is the most aggressive breast cancer subtype, characterized by limited treatment options and higher relapse rates than hormone-receptor-positive breast cancers. Chemotherapy remains the mainstay treatment for TNBC, and platinum salts have been explored as a therapeutic alternative in neo-adjuvant and metastatic settings. However, primary and acquired resistance to chemotherapy in general and platinum-based regimens specifically strongly hampers TNBC management. In this study, we used carboplatin-resistant in vivo patient-derived xenograft and isogenic TNBC cell-line models and detected enhanced Wnt/β-catenin activity correlating with an induced expression of stem cell markers in both resistant models. In accordance, the activation of canonical Wnt signaling in parental TNBC cell lines increases stem cell markers' expression, formation of tumorspheres and promotes carboplatin resistance. Finally, we prove that Wnt signaling inhibition resensitizes resistant models to carboplatin both in vitro and in vivo, suggesting the synergistic use of Wnt inhibitors and carboplatin as a therapeutic option in TNBC. Here we provide evidence for a prominent role of Wnt signaling in mediating resistance to carboplatin, and we establish that combinatorial targeting of Wnt signaling overcomes carboplatin resistance enhancing chemotherapeutic drug efficacy.
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