Posters
Presenting Author Academic/Professional Position
Undergraduate
Academic Level (Author 1)
Faculty
Discipline/Specialty (Author 1)
Neuroscience
Academic Level (Author 2)
Undergraduate
Discipline/Specialty (Author 2)
Neuroscience
Academic Level (Author 3)
Undergraduate
Discipline/Specialty (Author 3)
Neuroscience
Academic Level (Author 4)
Undergraduate
Discipline/Specialty (Author 4)
Neuroscience
Academic Level (Author 5)
Undergraduate
Discipline/Specialty (Author 5)
Neuroscience
Presentation Type
Poster
Discipline Track
Biomedical Science
Abstract Type
Research/Clinical
Abstract
Background: Glioblastoma multiforme (GBM) is the most common and lethal malignant primary brain tumor for which the development of efficacious chemotherapeutic agents remains an urgent need. In our previous studies, we demonstrated that niclosamide and camptothecin (CPT) synergistically suppressed the proliferation in human glioblastoma U87 MG cells. Recently, we observed that U87 MG cells failed to resume growth after the combined treatment was removed, a phenomenon not seen with either agent alone. We aimed to explore the sustained anti-tumor effects of niclosamide and CPT in GBM.
Methods: Human glioblastoma U87 MG cells were treated with 5 mM niclosamide, 5 mM CPT, or their combination. Cell proliferation was assessed using the MTT assay, apoptosis was detected via TUNEL assay, and cleaved caspase 3 activity was measured using Cellometer Spectrum.
Results: Following 24-hour drug treatment, the human glioblastoma cell line U87 MG was studied at 24 and 48 hours after the removal of the treatment. Niclosamide, CPT, and their combination significantly inhibited cell proliferation, with the combined treatment showing the most pronounced and sustained inhibitory effects. This enhanced inhibition was associated with increased apoptosis, driven by elevated levels of cleaved caspase 3 compared to single-agent treatments.
Conclusions: The combination of niclosamide and CPT exhibits potent and sustained anti-proliferative effects on GBM cells, mediated through enhanced apoptosis. These findings highlight its potential as a promising therapeutic strategy for GBM.
Recommended Citation
Fang, Xiaoqian; Ruiz, Araely; Yang, Eunseo; Morin, Brianna; Herrera-Toscano, Kimberly; Szobody, Megan; Fonseca, Josue; Osho, John-Beloved; and Lara, Raquel, "Uncovering the Mechanisms of Glioblastoma Relapse Prevention with Niclosamide and Camptothecin Treatment" (2025). Research Symposium. 21.
https://scholarworks.utrgv.edu/somrs/2025/posters/21
Included in
Cancer Biology Commons, Medicine and Health Sciences Commons, Molecular and Cellular Neuroscience Commons
Uncovering the Mechanisms of Glioblastoma Relapse Prevention with Niclosamide and Camptothecin Treatment
Background: Glioblastoma multiforme (GBM) is the most common and lethal malignant primary brain tumor for which the development of efficacious chemotherapeutic agents remains an urgent need. In our previous studies, we demonstrated that niclosamide and camptothecin (CPT) synergistically suppressed the proliferation in human glioblastoma U87 MG cells. Recently, we observed that U87 MG cells failed to resume growth after the combined treatment was removed, a phenomenon not seen with either agent alone. We aimed to explore the sustained anti-tumor effects of niclosamide and CPT in GBM.
Methods: Human glioblastoma U87 MG cells were treated with 5 mM niclosamide, 5 mM CPT, or their combination. Cell proliferation was assessed using the MTT assay, apoptosis was detected via TUNEL assay, and cleaved caspase 3 activity was measured using Cellometer Spectrum.
Results: Following 24-hour drug treatment, the human glioblastoma cell line U87 MG was studied at 24 and 48 hours after the removal of the treatment. Niclosamide, CPT, and their combination significantly inhibited cell proliferation, with the combined treatment showing the most pronounced and sustained inhibitory effects. This enhanced inhibition was associated with increased apoptosis, driven by elevated levels of cleaved caspase 3 compared to single-agent treatments.
Conclusions: The combination of niclosamide and CPT exhibits potent and sustained anti-proliferative effects on GBM cells, mediated through enhanced apoptosis. These findings highlight its potential as a promising therapeutic strategy for GBM.
