Deoxynivalenol induces apoptosis and autophagy in human prostate epithelial cells via PI3K/Akt signaling pathway

被引:0
作者
Karolina Kowalska
Marta Justyna Kozieł
Dominika Ewa Habrowska-Górczyńska
Kinga Anna Urbanek
Kamila Domińska
Agnieszka Wanda Piastowska-Ciesielska
机构
[1] Medical University of Lodz,
[2] Department of Cell Cultures and Genomic Analysis,undefined
[3] Medical University of Lodz,undefined
[4] Department of Comparative Endocrinology,undefined
来源
Archives of Toxicology | 2022年 / 96卷
关键词
Deoxynivalenol; Prostate; Apoptosis; Autophagy; Oxidative stress;
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学科分类号
摘要
Phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway is one of the most deregulated signaling pathway in prostate cancer. It controls basic processes in cells: cell proliferation and death. Any disturbances in the balance between cell death and survival might result in carcinogenesis. Deoxynivalenol (DON) is one of the most common mycotoxins, a toxic metabolites of fungi, present in our everyday diet and feed. Although previous studies reported DON to induce oxidative stress, modulate steroidogenesis, DNA damage and cell cycle modulation triggering together its toxicity, its effect on normal prostate epithelial cells is not known. The aim of the study was to evaluate the effect of DON on the apoptosis and autophagy in normal prostate epithelial cells via modulation of PI3K/Akt signaling pathway. The results showed that DON in a dose of 30 µM and 10 µM induces oxidative stress, DNA damage and cell cycle arrest in G2/M cell cycle phase. The higher concentration of DON induces apoptosis, whereas lower one autophagy in PNT1A cells, indicating that modulation of PI3K/Akt by DON results in the induction of autophagy triggering apoptosis in normal prostate epithelial cells.
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页码:231 / 241
页数:10
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