In vitro modulation and relationship between N-myc and HLA class I RNA steady-state levels in human neuroblastoma cells
Details
Serval ID
serval:BIB_BE9D21EAE1F0
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
In vitro modulation and relationship between N-myc and HLA class I RNA steady-state levels in human neuroblastoma cells
Journal
Cancer Research
ISSN
0008-5472
Publication state
Published
Issued date
12/1990
Peer-reviewed
Oui
Volume
50
Number
23
Pages
7532-6
Notes
In Vitro
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Dec 1
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Dec 1
Abstract
Neuroblastoma cell lines and tumors are characterized by low HLA class I expression. The majority of neuroblastoma cell lines and a high percentage of disseminated tumors display amplification of the nuclear protooncogene N-myc. An inverse correlation between HLA class I expression and N-myc amplification and overexpression has been recently described in neuroblastomas (NBs). In this study we have shown that cytokines (recombinant gamma-interferon, recombinant alpha-tumor necrosis factor), differentiation agents (dibutyryl cyclic AMP, phorbol myristate acetate) and growth factors (nerve growth factor, epithelial growth factor) were able to influence the growth rate and surface expression of HLA class I molecules as well as of a tumor-associated antigen on 2 representative NB cell lines. Induced decreased growth rate in NB cells was not always related to decreased N-myc expression. Analysis at the mRNA level revealed that both N-myc and HLA class I RNA steady-state levels could be modulated by several substances, including recombinant gamma-interferon, phorbol myristate acetate, dibutyryl cyclic AMP, and epithelial growth factor and were not necessarily linked. An inverse correlation between N-myc and HLA mRNA levels was observed only after exposure of NB cells to recombinant alpha-tumor necrosis factor. We conclude that N-myc and HLA class I RNA steady-state levels can be modulated independently and suggest that they are not necessarily inversely regulated.
Keywords
Blotting, Northern
Bucladesine/pharmacology
Epidermal Growth Factor/pharmacology
Gene Amplification
*Gene Expression Regulation, Neoplastic
Genes, myc
Histocompatibility Antigens Class I/*metabolism
Humans
Interferon Type II/pharmacology
Nerve Growth Factors/pharmacology
Neuroblastoma/*metabolism
Oncogene Protein p55(v-myc)/*biosynthesis
RNA/isolation & purification
Tetradecanoylphorbol Acetate
Tumor Necrosis Factor-alpha/pharmacology
Pubmed
Web of science
Create date
20/01/2008 16:55
Last modification date
20/08/2019 16:32