Open AccessC‐myc expression is maintained during the G 1 phase cell cycle block produced by beryllium
Author(s) -
Skilleter D. N.,
Barrass N. C.,
Price R. J.
Publication year - 1991
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/j.1365-2184.1991.tb01152.x
Subject(s) - cell cycle , cell division , gene expression , microbiology and biotechnology , biology , dna synthesis , in vitro , cell , oncogene , cell growth , chemistry , gene , biochemistry
. Salts of the toxic metal beryllium have been shown previously to prevent the synthesis of several enzymes essential for DN A replication in proliferating rat hepatic cells in vivo , and to inhibit the division of rat liver‐derived BL9L epithelial cells in vitro , specifically during the G 1 phase of the cell cycle. The present study shows, however, that exposure of serum‐stimulated sub‐confluent monolayer cultures of synchronized BL9L cells to inhibitory concentrations of the beryllium salt BeSO 4 (50 μm) did not impair expression of the cell proliferation associated nuclear proto‐oncogene c‐myc . On the contrary, the increased c‐myc mRNA levels normally observed during the G 1 phase were maintained by continuous exposure of the cells to BeSO 4 . This response was specific in that other colloid forming metal salts (ZnSO 4 and ZrSO 4 ), which did not inhibit cell division, had no affect on c‐myc expression, and mRNA levels for the constantly expressed H‐2Kb major histocompatibility complex gene (3'Kb) were unaltered by BeSO 4 treatment of the cells. The prevention by Be 2+ of the down‐regulation of c‐myc expression in serum‐stimulated BL9L cells appears to result from a modulation of the endogenous transcriptional control process for c‐myc , which allows a maintained expression of the gene.