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PMID: 8041712 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Participation of cyclin A in Myc-induced apoptosis.

Hoang AT, Cohen KJ, Barrett JF, Bergstrom DA, Dang CV

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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Article Info
Journal
Proceedings of the National Academy of Sciences of the United States of America
Abbr.
Proc Natl Acad Sci U S A
ISSN
0027-8424
Published
1994-07-19
Pages
6875-9
Language
English
Region
United States
NLM ID
7505876
PMCID
PMC44300
Subset
IM
Grants
NCI NIH HHS · CA51497 · United States
NCI NIH HHS · CA57341 · United States
NHLBI NIH HHS · T32HL07525 · United States
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