Emine Atas, PhD
MedUni Wien RESEARCHER OF THE MONTH June 2026
Prostate cancer (PCa) and Type 2 diabetes frequently co-occur, but their relationship is unclear. This study examined the impact of PPAR agonists on PCa tumorigenesis. High PPARG expression was associated with advanced disease and poor survival. The PPARγ agonists Pioglitazone and Tesaglitazar also reduced proliferation and PPARγ levels in primary and metastatic PCa cells. Proteomic analyses revealed metabolic differences between primary and metastatic PCa cells. Moreover, Pioglitazone shifted primary cells toward glycolysis and increased fatty acid oxidation in metastatic cells, lowering mitochondrial ATP production. It also suppressed migration and promoted an epithelial phenotype in primary PCa cells. In vivo, Pioglitazone reduced tumor growth in a metastatic xenograft model and altered AMPKα and mTOR signaling. Furthermore, diabetic PCa patients treated with PPAR agonists showed no biochemical recurrence over 5-10 years post-prostatectomy. Overall, Pioglitazone inhibits PCa progression and induces metabolic reprogramming, which highlights the potential of repurposing metabolic drugs for PCa therapy.
Selected Literature
- Atas, E. et al., The anti-diabetic PPARγ agonist Pioglitazone inhibits cell proliferation and induces metabolic reprogramming in prostate cancer. Mol. Cancer 24, 1–26 (2025).
- Pencik, J. et al. STAT3/LKB1 controls metastatic prostate cancer by regulating mTORC1/CREB pathway. Mol. Cancer 22, 133 (2023).
- Atas, E., Oberhuber, M. & Kenner, L. The Implications of PDK1–4 on Tumor Energy Metabolism, Aggressiveness and Therapy Resistance. Front. Oncol. 10, 1–9 (2020).
- Kalla, J. et al. Biobank of genetically defined murine prostate cancer tumoroids uncovers oncogenic pathways and drug vulnerabilities driven by PTEN-loss. 2025.03.14.643296 Preprint at https://doi.org/10.1101/2025.03.14.643296 (2025).