ArticleEXCLI journal2022
Cyclophosphamide and epirubicin induce high apoptosis in microglia cells while epirubicin provokes DNA damage and microglial activation at sub-lethal concentrations.
Article in EXCLI journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 18 citations in OpenAlex.
- Mesoporous-Shell Monolayer Plasmonic Architecture Enables Quantitative and Decision-Guided SERS.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting the pMHC-TCR Interaction: Molecular Strategies and Therapeutic Potential in Autoimmunity.International journal of molecular sciences · 2026Review
- Mechanistic insights and therapeutic interventions of mitochondrial quality control in chemotherapy-related cognitive impairment.Neoplasia (New York, N.Y.) · 2026Review
- Article
- Dietary Carvacrol Attenuates Cyclophosphamide-Induced Neurotoxicity: Implications for Food-Derived Neuroprotection and Molecular Mechanisms.Food science & nutrition · 2025Article
- A Novel Polyherbal Formulation Modulates Cyclophosphamide-Induced Cytotoxicity in TM3 Leydig Cells and Delays Fictive Ejaculation in Spinal Cord Transected Male Rats.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Hyaluronic Acid-Based Nanoparticles Loaded with Rutin as Vasculo-Protective Tools against Anthracycline-Induced Endothelial Damages.Pharmaceutics · 2024Article
- Repurposing proteasome inhibitors for improved treatment of triple-negative breast cancer.Cell death discovery · 2024Article
- Post-transplant cyclophosphamide-induced cardiotoxicity: A comprehensive review.Journal of cardiovascular and thoracic research · 2024Review
- Mesenchymal Stem Cells Target Gastric Cancer and Deliver EpirubicinCurrent stem cell research & therapy · 2024Article
- Epirubicin Treatment Induces Neurobehavioral, Oxido-Inflammatory and Neurohistology Alterations in Rats: Protective Effect of the Endogenous Metabolite of Tryptophan - 3-Indolepropionic Acid.Neurochemical research · 2023Article
- Psychological distress is involved in CRCI in breast cancer survivors via mediating cytokine levels.Cancer medicine · 2023Article
- The bovine dialyzable leukocyte extract, immunepotent CRP, synergically enhances cyclophosphamide-induced breast cancer cell death, through a caspase-independent mechanism.EXCLI journal · 2023Article
- Chemobrain in Breast Cancer: Mechanisms, Clinical Manifestations, and Potential Interventions.Drug safety · 2022Review
- Cerebral glucose changes after chemotherapy and their relation to long-term cognitive complaints and fatigue.Frontiers in oncology · 2022Article
- Combinatorial Effects of Chrysin with Doxorubicin, 5-Fluorouracil, and Cyclophosphamide on Triple-Negative Breast Cancer Cell Line.Iranian journal of pharmaceutical research : IJPRArticle
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemotherapy Related Cognitive Impairment (CRCI), also called chemobrain, diminishes cancer patient's life quality. Breast cancer (BC) patients have been described to be importantly affected, however, the mechanism leading to CRCI has not been fully elucidated. Recent research proposes microglia as the main architect of CRCI, thus dysregulations in these cells could trigger CRCI. The aim of this research was to evaluate the effects of two drugs commonly used against breast cancer, cyclophosphamide (CTX) and epirubicin (EPI), on the microglia cell line SIM-A9, using the BC cell line, 4T1, as a control. Our results show that CTX and EPI decrease microglia-cell viability and increase cell death on a concentration-dependent manner, being 5 and 2 times more cytotoxic to microglia cell line than to breast cancer 4T1cells, respectively. Both chemotherapies induce cell cycle arrest and a significant increase in p53, p16 and γ-H2AX in breast cancer and microglia cells. Furthermore, mitochondrial membrane potential (ΔΨm) diminishes as cell death increases, and both chemotherapies induce reactive oxygen species (ROS) production on SIM-A9 and 4T1. Moreover, caspase activation increases with treatments and its pharmacological blockade inhibits CTX and EPI induced-cell death. Finally, low concentrations of CTX and EPI induce γ-H2AX, and EPI induces cytokine release, NO production and Iba-1 overexpression. These findings indicate that microglia cells are more sensitive to CTX and EPI than BC cells and undergo DNA damage and cell cycle arrest at very low concentrations, moreover EPI induces microglia activation and a pro-inflammatory profile.
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