Posters
Presentation Type
Poster
Discipline Track
Clinical Science
Abstract Type
Research/Clinical
Abstract
Background. Chemotherapy Related Cognitive Impairment’s (CRCI), diminish patient’s quality life, being breast cancer (BC) patients the most affected. Microglia is described to play a major role in CRCI; hence, the aim of this research was to describe the cytotoxicity of cyclophosphamide (CTX) and Epirubicin (EPI), on microglia (SIM-A9), compared to BC cells (4T1).
Methods. We assessed cell viability (Resazurin) and cell death (AnnV), as well as nuclear damage with γ-H2AX, p53, p16 and cell cycle analysis (PI staining) by flow cytometry (FC). Furthermore, we evaluated ΔΨm (DIOC6), ROS (DCFDA) and NO (DAF-FM) production. Finally, caspase activation (TF2-VAD-FMK) and autophagy (CYTO-ID).
Results. Chemotherapies decrease microglia-cell viability and increase cell death in concentration dependent manner. Increases in p53, p16 and γ-H2AX and, cell cycle arrest was noted by CTX and EPI in SIMA-9 and 4T1 cells.Furthermore, Chemotherapy treatment induces, loss of ΔΨm, and ROS production on SIM-A9 and 4T1, demonstrating that NAC decreases EPI-induced cell death in SIM-A9 and CTX-induced in 4T1. Moreover, caspase activation increases with treatments and its pharmacological blockade inhibits CTX and EPI induced-cell death. Autophagosome formation was observed by EPI and CTX treatment in SIM-A9 as a protective mechanism. Lower EPI concentrations induced cell cycle arrest, γ-H2AX, NO production and pro-inflammatory cytokine release.
Conclusions. Chemotherapies induce higher cytotoxicity in microglia than in BC cells. ROS and caspase-dependent, as well as caspase dependent cell death was observed after EPI and CTX treatment in microglia respectively. Low concentrations of EPI induce DNA damage, NO production and cytokine dysregulation.
Academic/Professional Position
Graduate Student
Recommended Citation
de la Hoz-Camacho, Rafael, "Cyclophosphamide and Epirubicin Induce Apoptotic Cell Death In Microglia Cells" (2023). Research Symposium. 40.
https://scholarworks.utrgv.edu/somrs/theme1/posters/40
Included in
Cancer Biology Commons, Cell Biology Commons, Medicine and Health Sciences Commons, Molecular and Cellular Neuroscience Commons
Cyclophosphamide and Epirubicin Induce Apoptotic Cell Death In Microglia Cells
Background. Chemotherapy Related Cognitive Impairment’s (CRCI), diminish patient’s quality life, being breast cancer (BC) patients the most affected. Microglia is described to play a major role in CRCI; hence, the aim of this research was to describe the cytotoxicity of cyclophosphamide (CTX) and Epirubicin (EPI), on microglia (SIM-A9), compared to BC cells (4T1).
Methods. We assessed cell viability (Resazurin) and cell death (AnnV), as well as nuclear damage with γ-H2AX, p53, p16 and cell cycle analysis (PI staining) by flow cytometry (FC). Furthermore, we evaluated ΔΨm (DIOC6), ROS (DCFDA) and NO (DAF-FM) production. Finally, caspase activation (TF2-VAD-FMK) and autophagy (CYTO-ID).
Results. Chemotherapies decrease microglia-cell viability and increase cell death in concentration dependent manner. Increases in p53, p16 and γ-H2AX and, cell cycle arrest was noted by CTX and EPI in SIMA-9 and 4T1 cells.Furthermore, Chemotherapy treatment induces, loss of ΔΨm, and ROS production on SIM-A9 and 4T1, demonstrating that NAC decreases EPI-induced cell death in SIM-A9 and CTX-induced in 4T1. Moreover, caspase activation increases with treatments and its pharmacological blockade inhibits CTX and EPI induced-cell death. Autophagosome formation was observed by EPI and CTX treatment in SIM-A9 as a protective mechanism. Lower EPI concentrations induced cell cycle arrest, γ-H2AX, NO production and pro-inflammatory cytokine release.
Conclusions. Chemotherapies induce higher cytotoxicity in microglia than in BC cells. ROS and caspase-dependent, as well as caspase dependent cell death was observed after EPI and CTX treatment in microglia respectively. Low concentrations of EPI induce DNA damage, NO production and cytokine dysregulation.