蛋白激酶B
自噬
PI3K/AKT/mTOR通路
细胞凋亡
细胞生物学
程序性细胞死亡
信号转导
生物
细胞周期
癌症研究
DNA损伤
癌变
氧化应激
磷酸肌醇3激酶
化学
内分泌学
癌症
生物化学
DNA
遗传学
作者
Karolina Kowalska,Marta Justyna Kozieł,Dominika Ewa Habrowska-Górczyńska,Kinga Anna Urbanek,Kamila Domińska,Agnieszka Wanda Piastowska-Ciesielska
标识
DOI:10.1007/s00204-021-03176-z
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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