ArticleBritish journal of pharmacology2020
Modeling Neoadjuvant chemotherapy resistance in vitro increased NRP-1 and HER2 expression and converted MCF7 breast cancer subtype.
Article in British journal of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Improving Laboratory-Based Cancer Drug Discovery Study Designs for Better Research Translations.Methods and protocols · 2026Review
- HER2-Low Breast Cancer: Biological Framework and Determinants of HER2 Instability.Medicina (Kaunas, Lithuania) · 2026Review
- Erbin Inhibited AngiogenesisCurrent medicinal chemistry · 2026Article
- Research advancements in nanoparticles and cell-based drug delivery systems for the targeted killing of cancer cells.Oncology research · 2025Review
- Review
- Glycemic load impacts the response of acquired resistance in breast cancer cells to chemotherapeutic drugs in vitro.PloS one · 2024Article
- Neuropilin-1 Knockout and Rescue Confirms Its Role to Promote Metastasis in MDA-MB-231 Breast Cancer Cells.International journal of molecular sciences · 2023Article
- Long noncoding RNA RP11-70C1.3 confers chemoresistance of breast cancer cells through miR-6736-3p/NRP-1 axis.Bosnian journal of basic medical sciences · 2022Article
- Modeling Neoadjuvant chemotherapy resistance in vitro increased NRP-1 and HER2 expression and converted MCF7 breast cancer subtype.British journal of pharmacology · 2020Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
background and purposePatients with locally advanced breast cancer usually receive third-generation neoadjuvant chemotherapy (NAC). Although NAC treatment improved the overall survival, patients' response varies, some acquire resistance and others exhibit a conversion in their breast cancer molecular subtype. We aimed to identify the molecular changes involved in NAC resistance attempting to find new therapeutic targets in different breast cancer subtypes. EXPERIMENTAL APPROACH: We modelled NAC treatments used in clinical practice and generated resistant cell lines in vitro. The resistant cells were generated by consecutive treatment with four cycles of doxorubicin (adriamycin)/cyclophosphamide (4xAC) followed by an additional four cycles of paclitaxel (4xAC + 4xPAC). KEY
resultsOur data revealed distinct mechanisms of resistance depending on breast cancer subtype and drugs used. MDA-MB-231 cells resistant to 4xAC + 4xPAC activated neuropilin-1/TNC/integrin β3/FAK/NF-κB CONCLUSIONS AND IMPLICATIONS: The concurrent increase in neuropilin-1 and HER2 upon resistance and the inverse relationship between neuropilin-1 and BCRP/ABCG2 suggest that, in addition to HER2, neuropilin-1 status should be assessed in patients undergoing NAC, and as a potential drug target for refractory breast cancer.
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