In vitro modulation and relationship between N-myc and HLA class I RNA steady-state levels in human neuroblastoma cells

Détails

ID Serval
serval:BIB_BE9D21EAE1F0
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
In vitro modulation and relationship between N-myc and HLA class I RNA steady-state levels in human neuroblastoma cells
Périodique
Cancer Research
Auteur⸱e⸱s
Gross  N., Beck  D., Favre  S.
ISSN
0008-5472
Statut éditorial
Publié
Date de publication
12/1990
Peer-reviewed
Oui
Volume
50
Numéro
23
Pages
7532-6
Notes
In Vitro
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Dec 1
Résumé
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.
Mots-clé
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
Création de la notice
20/01/2008 15:55
Dernière modification de la notice
20/08/2019 15:32
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