蛋白激酶B
PI3K/AKT/mTOR通路
膜联蛋白
细胞凋亡
细胞生物学
激酶
蛋白激酶A
信号转导
细胞周期
分子生物学
生物
酪氨酸激酶
化学
癌症研究
生物化学
作者
Reena Kasi,Chye Soi Moi,Yip Wai Kien,Koh Rhun Yian,Ng Wei Chin,Ng Khuen Yen,Gnanajothy Ponnudurai,Seow Heng Fong
出处
期刊:Molecular Medicine Reports
[Spandidos Publications]
日期:2014-11-19
卷期号:11 (3): 2262-2268
被引量:5
标识
DOI:10.3892/mmr.2014.2979
摘要
para‑Phenylenediamine (p‑PD) is a potential carcinogen, and widely used in marketed hair dye formulations. In the present study, the role of the protein tyrosine kinase (PTK)/Ras/Raf/c‑Jun N‑terminal kinase (JNK) and phosphoinositide 3‑kinase (PI3k)/protein kinase B (Akt) pathways on the growth of NRK‑52E cells was investigated. The results demonstrated that p‑PD reduced cell viability in a dose‑dependent manner. The cell death due to apoptosis was confirmed by cell cycle analysis and an Annexin‑V‑fluorescein isothiocyanate binding assay. Subsequent to staining with 2',7'‑dichlorofluorescin diacetate, the treated cells demonstrated a significant increase in reactive oxygen species (ROS) generation compared with the controls. The effects of p‑PD on the signalling pathways were analysed by western blotting. p‑PD‑treated cells exhibited an upregulated phospho‑stress‑activated protein kinase/JNK protein expression level and downregulated Ras and Raf protein expression levels; however, Akt, Bcl‑2, Bcl‑XL and Bad protein expression levels were not significantly altered compared with the control. In conclusion, p‑PD induced apoptosis by a PTK/Ras/Raf/JNK‑dependent pathway and was independent of the PI3K/Akt pathway in NRK‑52E cells.
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