Korean J Phys Anthropol.  2007 Dec;20(4):331-342.

Fenretinide Induced Apoptosis in Human Neuroblastoma Cell Lines

Affiliations
  • 1Department of Biochemistry and Molecular Biology, College of Medicine, Yeungnam University, Daegu, Korea. seongyong@med.yu.ac.kr
  • 2Department of Anatomy, College of Medicine, Yeungnam University, Daegu, Korea.
  • 3Department of Neurosurgery, Masan Bokeum Hospital, Korea.

Abstract

Retinoids play an important role in growth, reproduction and differentiation. Recently, retinoids have been used to both protect and treat from various animal models of carcinogenesis. In this study the effect of N-(4-hydroxyphenyl) retinamide (fenretinide) on viability of human neuroblastoma cell lines were evaluated. For the evaluation of apoptosis of human neuroblastoma cell lines by fenretinide. MTT assay, cytoplasmic DNA fragmentation, TUNEL stain, and Western blot analysis were performed. In MTT assay, fenretinide inhibited the proliferation of CHP134, IMR32 and SH-SY5Y but not in PC12 cells. Cytoplasmic DNA fragmentation was induced by treament of fenretinide (10 micrometer) for 48 h in IMR32 cells. PARP cleavage was detected by Western blot analysis after 16 h of treatment of fenretinide in CHP134, IMR32 and SH-SY5Y. These fenretinide effects on growth inhibition and increased apoptosis followed to the time dependent manner. The fenretinide treatment did not affect the phosphorylation of MAP kinases (ERK, JNK, p38). There was no change of Bcl-x and Bad expression after treatment of fenretinide (1 micrometer) in neroblastoma cell lines. Pretreatement of PD98059, SB203580, LY294002, or genistein also did not affect fenretinide-induced PARP cleavage in neuroblastoma cell lines. From these results, the fenretinide-induced apoptosis is due to the PARP cleavage which occured MAP kinase signal cascades independently.

Keyword

Apoptosis; Fenretinide; Human neuroblastoma cell line; MAP kinase; Retinoids

MeSH Terms

Animals
Apoptosis*
Blotting, Western
Carcinogenesis
Cell Line*
Cytoplasm
DNA Fragmentation
Fenretinide*
Genistein
Humans*
In Situ Nick-End Labeling
Models, Animal
Neuroblastoma*
PC12 Cells
Phosphorylation
Phosphotransferases
Reproduction
Retinoids
Fenretinide
Genistein
Phosphotransferases
Retinoids
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