SFEIES24 Poster Presentations Adrenal & Cardiovascular (40 abstracts)
Hyperthermia-induced cell death in adrenocortical carcinoma: efficacy and mechanisms beyond caspase 3 apoptosis
Nathan Mullen 1 , Padraig T. Donlon 1 , Sarah Feely 1 , Anna Sorushanova 1 , Ritihaas Challapalli 1 , Kate M. Warde 1,2 , Cong Hong 1 , Punit Prakash 3 , Martin O’Halloran 4 & Michael Conall Dennedy 1
1Discipline of Pharmacology and Therapeutics, School of Medicine, University of Galway, Galway, Ireland; 2Huntsman Cancer Institute, Department of Oncological Sciences, University of Utah School of Medicine, Utah, USA; 3Department of Electrical and Computer Engineering, Kansas State University, Manhattan, USA; 4Translational Medical Device Laboratory, University of Galway, Galway, Ireland
Adrenocortical carcinoma (ACC) is a rare, aggressive cancer with notable resistance to conventional therapies. Despite advancements in medical research, understanding the mechanisms behind ACC’s resilience and exploring novel therapeutic strategies remain underdeveloped. Hyperthermia, the exposure of body tissue to high temperatures, is a potential treatment. However, the fundamental principles of how hyperthermia induces cell death in ACC are not well understood. This study aimed to address this gap by investigating hyperthermia’s effectiveness in inducing cell death in ACC cells and examining the potential role of Caspase-3 mediated apoptosis.
Methods: The ACC cell lines (H295R and HAC15) and the non-cancerous HUVEC endothelial cell line were treated with hyperthermia at 42°C, 45°C, 48°C, and 50°C using temperature-controlled water baths. Cell viability was assessed using Annexin V/Sytox blue (flow cytometry), Calcein/Propidium iodide (confocal microscopy), and the xCELLigence Real Time Cell Analyser. The involvement of Caspase-3 mediated apoptosis was evaluated through western blotting.
Results: Significant reductions in cell viability were observed in H295R and HAC15 cells at 48°C and 50°C, both immediately and 24 hours post-treatment, defining these temperatures as ’lethal’ for ACC cells. HUVEC cells were more robust at all treatment temperatures, indicating varied cellular sensitivities to hyperthermia. At 45°C, ACC cells initially showed decreased viability, with less cell death seen 24 hours post-treatment, suggesting an adaptive response to sublethal hyperthermic stress. Results from Annexin V/Sytox Blue staining and Caspase-3 western blotting indicated that Caspase-3 mediated apoptosis was not the primary pathway for hyperthermia-induced cell death in ACC cells.
Conclusion: Hyperthermia at temperatures ≥48°C is lethal to ACC cells, presenting new therapeutic possibilities. However, ACC cells show resilience at 45°C, suggesting alternative mechanisms beyond Caspase-3 mediated apoptosis in hyperthermia-induced cell death.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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