Abstract
The involvement of c-Myc in cellular proliferation or apoptosis has been linked to differential cyclin gene expression. We observed that in both proliferating cells and cells undergoing apoptosis, cyclin A (but not B, C, D1, and E) mRNA level was elevated in unsynchronized Myc-overexpressing cells when compared with parental Rat1a fibroblasts. We further demonstrated that Zn(2+)-inducible cyclin A expression was sufficient to cause apoptosis. When Myc-induced apoptosis was blocked by coexpression of Bcl-2, the levels of cyclin C, D1, and E mRNAs were also elevated. Thus, while apoptosis induced by c-Myc is associated with an elevated cyclin A mRNA level, protection from apoptosis by coexpressed Bcl-2 is associated with a complementary increase in cyclin C, D1, and E mRNAs.
MeSH Terms
Animals
Apoptosis
Cell Division
Cell Line
Cyclins/genetics,physiology
Gene Expression Regulation
Humans
Proto-Oncogene Proteins c-myc/physiology
RNA, Messenger/metabolism
Rats
Transfection
Zinc/pharmacology
Chemicals
Cyclins
Proto-Oncogene Proteins c-myc
RNA, Messenger
Zinc
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Hoang A T
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Cohen K J
Barrett J F
Bergstrom D A
Dang C V
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