P73 | ANALYSIS OF SAPK/JNK PATHWAY IN DOXORUBICIN INDUCED ADIPOSE-DERIVED STEM CELL CYTOTOXICITY
A. Skubis-Sikora, B. Sikora, K. Pogoda-Mieszczak, E. Bogunia, P. Czekaj | Department of Cytophysiology, Chair of Histology and Embryology, Faculty of Medical Sciences in Katowice, Medical University of Silesia in Katowice, Poland
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Doxorubicin (DOX) is a member of the anthracycline group of chemotherapy drugs, which have a broad spectrum of activity. Its mechanism is based on intercalation into cancer cell DNA. However, DOX also exerts harmful effects on normal tissues, contributing to adverse outcomes such as cardiotoxicity. Furthermore, it has been demonstrated that DOX can lead to damage stem cell populations, thereby impairing their regenerative capacity1. Despite extensive research, the mechanisms by which DOX acts on mesenchymal stem cells (MSCs) and the potential strategies to protect them remain to be fully elucidated. It is likely that the SAPK/ JNK (Stress-activated protein kinases/Jun amino-terminal kinases) pathway plays a crucial role in malignancy and resistance of cancer cells2. The study’s objective was to evaluate the cytotoxic effect of DOX on adipose-derived stem cells (ADSCs), and to analyze whether SAPK/ JNK expression is associated with this process. The viability of ADSCs was evaluated at concentrations of DOX, ranging from 0.1 µM to 100 µM after 24-h incubation period. Three concentrations were selected for further experiments. The cells were then analyzed for gene and protein expression related to the SAPK/JNK pathway. It was observed that there was a decrease in cell viability in a dose-dependent manner following treatment with DOX at concentrations of 5 µM and above. Furthermore, DOX has been shown to modify the expression of SAPK/JNK-related genes and to protein levels. The study concluded that SAPK/JNK pathway undergoes alterations in response to DOX treatment and it can play a role in activating the stress response to DOX exposure.
The study was supported by grants no. 2023/07/X/NZ3/00379, BNW-2-013/K/4/I and SKN/SP/601468/2024.
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