Evidence map›Paper›PMID 10871348›Full record

ArticleNucleic acids research2000

Activation of the myc oncoprotein leads to increased turnover of thrombospondin-1 mRNA.

A Janz, C Sevignani, K Kenyon, C V Ngo, A Thomas-Tikhonenko

Open access · bronzeAbstract read
In one paragraph

Article in Nucleic acids research, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.3field-weighted citation impact, top 19% of its field
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

37 citing papers in PubMed, 88 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Functions of Thrombospondin-1 in the Tumor Microenvironment.International journal of molecular sciences · 2021
    Review
  5. Idiopathic Pulmonary Comorbidities and Mechanisms.International journal of inflammation · 2021
    Review
  6. THBS1 (thrombospondin-1).Atlas of genetics and cytogenetics in oncology and haematology · 2020
    Article
  7. HIF-1α represses the expression of the angiogenesis inhibitor thrombospondin-2.Matrix biology : journal of the International Society for Matrix Biology · 2018
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Invoking the power of thrombospondins: regulation of thrombospondins expression.Matrix biology : journal of the International Society for Matrix Biology · 2014
    Review
  14. Review
  15. MYC and the art of microRNA maintenance.Cold Spring Harbor perspectives in medicine · 2014
    Review
  16. Review
  17. Oncogenes and angiogenesis: a way to personalize anti-angiogenic therapy?Cellular and molecular life sciences : CMLS · 2013
    Review
  18. Article
  19. Review
  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

5 authors at 1 institution in 1 country.

A JanzTechnische Universität Braunschweig, D-38023 Braunschweig, Germany,
C Sevignani
K Kenyon
C V Ngo
A Thomas-Tikhonenko
Technische Universität Braunschweig · DE

Funding

CONTROL OF THE THROMBOSPONDIN-1 GENE BY MYC ONCOPROTEINSR29CA071881 · NCI · UNIVERSITY OF PENNSYLVANIA · PI THOMAS-TIKHONENKO, ANDREI · 1997 to 2001
$281k
NCI NIH HHS R29 CA71881N
6 · The paper itself

Abstract

The Myc oncoprotein is implicated in transcriptional regulation of a variety of genes pertaining to cell cycle and neoplastic transformation. Examples of both positive and negative regulation have been reported that involve E-box and initiator (Inr) promoter elements, respectively. In both cases, Myc is thought to induce changes in transcription initiation. We have previously shown that overexpression of Myc causes down-regulation of the thrombospondin-1 (tsp-1) gene, an important negative modulator of tumor angiogenesis. In this study, we demonstrate that Myc in combination with Max can bind, albeit with low affinity, to an E-box-like element in the tsp-1 promoter. However, the 2.7 kb DNA segment containing both this non-canonical E-box and an Inr-like sequence does not constitute a Myc-responsive element in a transient expression system. Furthermore, Myc does not significantly affect the rate of initiation or elongation of the tsp-1 mRNA. Thus, in this instance Myc does not act as a canonical transcription factor. Instead, as demonstrated by blocking de novo RNA synthesis, down-regulation of the tsp-1 gene by Myc occurs through increased mRNA turnover. To our knowledge, this is the first example of gene regulation by Myc that involves mRNA destabilization.

Indexed as

Transcription FactorsAnimalsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsBasic-Leucine Zipper Transcription FactorsCells, CulturedDNA-Binding ProteinsGene Expression RegulationGenes, ReporterPromoter Regions, GeneticProto-Oncogene Proteins c-mycRatsRegulatory Sequences, Nucleic AcidRNA, MessengerThrombospondin 1TransfectionBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsBasic-Leucine Zipper Transcription FactorsDNA-Binding ProteinsMax protein, ratMyc associated factor XProto-Oncogene Proteins c-mycRNA, MessengerThrombospondin 1Transcription Factors

Identifiers

PMID10871348
PMCPMC102633
OpenAlexW2132318673

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.