Posters
Presenting Author Academic/Professional Position
Postdoctoral fellow
Academic Level (Author 1)
Post-doc
Discipline/Specialty (Author 1)
Cancer and Immunology
Academic Level (Author 2)
Staff
Discipline/Specialty (Author 2)
Cancer and Immunology
Academic Level (Author 3)
Post-doc
Discipline/Specialty (Author 3)
Cancer and Immunology
Academic Level (Author 4)
Post-doc
Discipline/Specialty (Author 4)
Cancer and Immunology
Academic Level (Author 5)
Staff
Discipline/Specialty (Author 5)
Cancer and Immunology
Discipline Track
Biomedical Science
Abstract Type
Research/Clinical
Abstract
Aim: Repurposing of FDA-approved antifungal drugs to combat prostate cancer.
Background: Prostate cancer is one of the leading causes of cancer death among men in the United States, second only to non-melanoma skin cancer. The American Cancer Society estimates about 313,780 new cases and 35,770 deaths from prostate cancer in 2025. Despite various treatments such as radiation therapy (both external beam and internal), chemotherapy, hormone therapy, cryotherapy, biological therapy, and high-intensity focused ultrasound, men are monitored for side effects over many years. Therefore, new drugs and treatment strategies are urgently needed to address this challenge.
Methods: In this study, we performed a CCK-8 assay, colony formation assay, and invasion and migration assays with the tested drugs to identify the most potent one that can reduce prostate cancer. The anti-apoptotic property of miconazole was evaluated by follow-up confocal and scanning electron microscopy, flow cytometry, and Western blotting techniques. Further, we performed proteomic analysis to identify the lead proteins responsible for cell cycle regulation and apoptosis in prostate cancer cells, followed by a pathway enrichment analysis to identify the top disease pathways and respective signaling mechanisms.
Results: Miconazole showed significant inhibition of prostate cancer cells compared to other antifungal drugs, as evident from cck-8 assay, colony formation assay, and invasion and migration assays. Confocal and scanning electron microscopy, flow cytometry, and Western blotting analysis revealed that miconazole induced morphological changes in the cells and nuclei, arrested cell cycle at G0/G1 phase by downregulating cyclin D3, CDK2, CDK4, and PCNA, and induced significant apoptosis by upregulating p53, p21, p27, cl-PARP, cl-caspase-3, and downregulating PARP-1 and caspase-3 expression levels, in prostate cancer cells. Further, proteomic analysis revealed that miconazole significantly regulated many proteins responsible for cell cycle arrest and apoptosis.
Conclusions: These findings from the drug repurposing strategy may provide a novel approach to the discovery of new drugs and their combinations, in the future, to fight against prostate cancer.
Presentation Type
Poster
Recommended Citation
Ghali, Eswara Naga Hanuma Kumar; Shim, Lindsey; Tiwari, Rahul; Baru, Rajasekhar; Dhasmana, Anupam; Chang, Ryan; Jung, Sung Yun; Kashyap, Vivek K.; Chauhan, Neeraj; Chauhan, Subhash; and Yallapu, Murali, "Miconazole induces cell cycle arrest and apoptosis in prostate cancer cells via a p53-mediated pathway: A Drug repurposing strategy" (2025). Research Colloquium. 40.
https://scholarworks.utrgv.edu/colloquium/2025/posters/40
Included in
Miconazole induces cell cycle arrest and apoptosis in prostate cancer cells via a p53-mediated pathway: A Drug repurposing strategy
Aim: Repurposing of FDA-approved antifungal drugs to combat prostate cancer.
Background: Prostate cancer is one of the leading causes of cancer death among men in the United States, second only to non-melanoma skin cancer. The American Cancer Society estimates about 313,780 new cases and 35,770 deaths from prostate cancer in 2025. Despite various treatments such as radiation therapy (both external beam and internal), chemotherapy, hormone therapy, cryotherapy, biological therapy, and high-intensity focused ultrasound, men are monitored for side effects over many years. Therefore, new drugs and treatment strategies are urgently needed to address this challenge.
Methods: In this study, we performed a CCK-8 assay, colony formation assay, and invasion and migration assays with the tested drugs to identify the most potent one that can reduce prostate cancer. The anti-apoptotic property of miconazole was evaluated by follow-up confocal and scanning electron microscopy, flow cytometry, and Western blotting techniques. Further, we performed proteomic analysis to identify the lead proteins responsible for cell cycle regulation and apoptosis in prostate cancer cells, followed by a pathway enrichment analysis to identify the top disease pathways and respective signaling mechanisms.
Results: Miconazole showed significant inhibition of prostate cancer cells compared to other antifungal drugs, as evident from cck-8 assay, colony formation assay, and invasion and migration assays. Confocal and scanning electron microscopy, flow cytometry, and Western blotting analysis revealed that miconazole induced morphological changes in the cells and nuclei, arrested cell cycle at G0/G1 phase by downregulating cyclin D3, CDK2, CDK4, and PCNA, and induced significant apoptosis by upregulating p53, p21, p27, cl-PARP, cl-caspase-3, and downregulating PARP-1 and caspase-3 expression levels, in prostate cancer cells. Further, proteomic analysis revealed that miconazole significantly regulated many proteins responsible for cell cycle arrest and apoptosis.
Conclusions: These findings from the drug repurposing strategy may provide a novel approach to the discovery of new drugs and their combinations, in the future, to fight against prostate cancer.
