Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comparative Study
. 1989 May;86(9):3379-83.
doi: 10.1073/pnas.86.9.3379.

An oligomer complementary to c-myb-encoded mRNA inhibits proliferation of human myeloid leukemia cell lines

G Anfossi  1 , A M Gewirtz, B Calabretta
Affiliations
Comparative Study

An oligomer complementary to c-myb-encoded mRNA inhibits proliferation of human myeloid leukemia cell lines

G Anfossi et al. Proc Natl Acad Sci U S A. 1989 May.

Abstract

To study the role of the protooncogene c-myb in regulating myeloid leukemia cell proliferation and differentiation, we exposed cells of the human leukemia lines HL-60, ML-3, KG-1, and KG-1a to an oligodeoxynucleotide complementary to an 18-base-pair (bp) sequence of c-myb-encoded mRNA. This treatment resulted in a significant decrease in cell proliferation in all of the lines, which was most marked in HL-60 cells. After 5 days in culture, in several separate experiments with different oligomer preparations, 75% growth inhibition was observed in c-myb antisense treated cells in comparison to untreated HL-60 cells. Two c-myb antisense oligomers of identical length with either 2- or 4-bp mismatches had no effect on cell growth nor did an 18-bp c-myb sense or myeloperoxidase antisense oligomer. The effect of a c-myc antisense oligomer (18 bp) on the growth of HL-60, KG-1, and KG-1a cells was also studied. This oligomer had much less inhibitory effect on cell proliferation than did the c-myb antisense sequence. Interestingly, although c-myc antisense treatment induced maturation of HL-60 cells while it inhibited cell proliferation, such an effect was not noted in c-myb antisense treated cells. These studies indicate that the nuclear protein encoded by the c-myb protooncogene is required for maintenance of proliferation in certain leukemia cell lines. In compared to c-myc protein suggest that, at least in HL-60 cells, c-myc amplification or N-ras activation may not be sufficient to maintain the leukemic growth in the absence of c-myb protein. These findings support the hypothesis that development and maintenance of a malignant phenotype requires a multiplicity of interrelated genetic events.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Nature. 1977 Nov 24;270(5635):347-9 - PubMed
    1. Science. 1988 Dec 2;242(4883):1303-6 - PubMed
    1. Proc Natl Acad Sci U S A. 1978 Jan;75(1):285-8 - PubMed
    1. Science. 1978 Jun 9;200(4346):1153-4 - PubMed
    1. J Exp Med. 1979 Apr 1;149(4):969-74 - PubMed

Publication types

MeSH terms