NDLI: Para-phenylenediamine-induces apoptosis via a pathway dependent on PTK-Ras-Raf-JNK activation but independent of the PI3K/Akt pathway in NRK-52E cells.

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Para-phenylenediamine-induces apoptosis via a pathway dependent on PTK-Ras-Raf-JNK activation but independent of the PI3K/Akt pathway in NRK-52E cells.

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Para-phenylenediamine-induces apoptosis via a pathway dependent on PTK-Ras-Raf-JNK activation but independent of the PI3K/Akt pathway in NRK-52E cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Yen, Ng Khuen Moi, Chye Soi Yian, Koh Rhun Ponnudurai, Gnanajothy Kien, Yip Wai Fong, Seow Heng Chin, Ng Wei Kasi, Reena A. P.
Description	Country affiliation: Malaysia Author Affiliation: Kasi RA ( Department of Human Biology, Cells and Molecules, International Medical University, Kuala Lumpur 57000, Malaysia.); Moi CS ( Department of Human Biology, Cells and Molecules, International Medical University, Kuala Lumpur 57000, Malaysia.); Kien YW ( Department of Pathology, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Serdang, Selangor 43400, Malaysia.); Yian KR ( Department of Human Biology, Cells and Molecules, International Medical University, Kuala Lumpur 57000, Malaysia.); Chin NW ( Department of Human Biology, Cells and Molecules, International Medical University, Kuala Lumpur 57000, Malaysia.); Yen NK ( Jeffrey Cheah School of Medicine and Health Sciences, Monash University Sunway Campus, Bandar Sunway, Selangor 47500, Malaysia.); Ponnudurai G ( Department of Human Biology, Cells and Molecules, International Medical University, Kuala Lumpur 57000, Malaysia.); Fong SH ( Department of Pathology, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Serdang, Selangor 43400, Malaysia.)
Abstract	paraPhenylenediamine (pPD) 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/cJun Nterminal kinase (JNK) and phosphoinositide 3kinase (PI3k)/protein kinase B (Akt) pathways on the growth of NRK52E cells was investigated. The results demonstrated that pPD reduced cell viability in a dosedependent manner. The cell death due to apoptosis was confirmed by cell cycle analysis and an AnnexinVfluorescein 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 pPD on the signalling pathways were analysed by western blotting. pPDtreated cells exhibited an upregulated phosphostressactivated protein kinase/JNK protein expression level and downregulated Ras and Raf protein expression levels; however, Akt, Bcl2, BclXL and Bad protein expression levels were not significantly altered compared with the control. In conclusion, pPD induced apoptosis by a PTK/Ras/Raf/JNKdependent pathway and was independent of the PI3K/Akt pathway in NRK52E cells.
ISSN	17912997
e-ISSN	17913004
Journal	Molecular Medicine Reports
Issue Number	3
Volume Number	11
Language	English
Publisher	Spandidos Publications
Publisher Date	2015-03-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Apoptosis Drug Effects Phenylenediamines Pharmacology Signal Transduction Animals Annexin A5 Metabolism Cell Cycle Cell Line Cell Survival Jnk Mitogen-activated Protein Kinases Mitosis Phosphatidylinositol 3-kinases Proto-oncogene Proteins C-akt Proto-oncogene Proteins C-bcl-2 Proto-oncogene Proteins C-raf Proto-oncogene Proteins P21(ras) Reactive Oxygen Species Bcl-associated Death Protein Bcl-x Protein Research Support, Non-u.s. Gov't Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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