Evidence map›Paper›PMID 8421701›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1993

Inhibitory effects of antisense oligodeoxynucleotides targeting c-myc mRNA on smooth muscle cell proliferation and migration.

S Biro, Y M Fu, Z X Yu, S E Epstein

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Delivery of oligonucleotides with lipid nanoparticles.Advanced drug delivery reviews · 2015
    Review
  6. Article
  7. Incorporation of two modified nucleosides allows selective platination of an oligonucleotide making it suitable for duplex cross-linking.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2007
    Article
  8. Article
  9. Article
  10. Article
  11. An in vivo function for the transforming Myc protein: elicitation of the angiogenic phenotype.Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research · 2000
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Phosphorothioate Oligodeoxynucleotide Inhibition of Restenosis.Journal of thrombosis and thrombolysis · 1998
    Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

S BiroCardiology Branch, National Heart, Lung, and Blood Institute, Bethesda, MD 20892.
Y M Fu
Z X Yu
S E Epstein

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Smooth muscle cell (SMC) proliferation and migration play pivotal roles in restenosis following angioplasty. c-myc is an immediate early response gene induced by various mitogens, and several lines of evidence derived from experiments using transformed or hematopoietic cell lines, or transgenic mice, suggest its protein product plays a role in numerous signaling transduction pathways, including those modulating cell division. We therefore reasoned that a strategy employing oligodeoxynucleotides (ODNs) complementary to c-myc mRNA (antisense ODNs) might be potent inhibitors of SMC proliferation and, perhaps, of SMC migration. To evaluate this concept, we tested several antisense ODNs targeted to c-myc mRNA (15- or 18-mer ODNs complementary to different c-myc mRNA sequences) by introducing them individually into the medium of cultured rat aortic SMCs. Phosphoroamidate-modified ODNs were employed to retard degradation. Antisense ODNs inhibited, in a concentration-dependent manner, SMC proliferation and SMC migration. Maximal inhibitory effect was 50% for proliferation and > 90% for migration. These effects were associated with decreased SMC expression of c-myc-encoded protein by Western immunoblotting and immunocytochemical staining. ODNs with the same nucleotides but a scrambled sequence caused no effect. These results indicate that the c-myc gene product is involved in the signal transduction pathways mediating SMC proliferation and migration in the in vitro model we employed. The results also suggest a potential role of antisense strategies designed to inhibit c-myc expression for the prevention of coronary restenosis.

Indexed as

AnimalsBase SequenceCell DivisionCell MovementCells, CulturedDose-Response Relationship, DrugGenes, mycImmunohistochemistryMolecular Sequence DataMuscle DevelopmentMuscle, SmoothOligodeoxyribonucleotidesOligonucleotides, AntisenseProto-Oncogene Proteins c-mycRatsRats, Sprague-DawleyOligodeoxyribonucleotidesOligonucleotides, AntisenseProto-Oncogene Proteins c-mycRNA, Messenger

Identifiers

PMID8421701
PMCPMC45722

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.