Evidence map›Paper›PMID 28806396›Full record

ArticleOncogene2017

Inhibiting MYC binding to the E-box DNA motif by ME47 decreases tumour xenograft growth.

L C Lustig, D Dingar, W B Tu, C Lourenco, M Kalkat, I Inamoto, R Ponzielli, W C W Chan, J A Shin, L Z Penn

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 44 citations in OpenAlex.

  1. Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026
    Review
  2. Review
  3. Review
  4. Review
  5. Beyond the Limit: MYC Mediates Tumor Immune Escape.Pharmaceuticals (Basel, Switzerland) · 2025
    Review
  6. Article
  7. Article
  8. Demystifying the Druggability of the MYC Family of Oncogenes.Journal of the American Chemical Society · 2023
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
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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

10 authors at 3 institutions in 1 country.

L C LustigPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
D DingarPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
W B TuPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
C LourencoPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
M KalkatPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
I InamotoDepartment of Chemistry, University of Toronto, Toronto, ON, Canada.
R PonzielliPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
W C W ChanInstitute of Biomaterials and Biomedical Engineering, University of Toronto, Donnelly Centre for Cellular and Biomolecular Research, Department of Materials Science and Engineering, Department of Chemical Engineering, Toronto, ON, Canada.
J A ShinDepartment of Chemistry, University of Toronto, Toronto, ON, Canada.
L Z PennPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
University Health Network · CAUniversity of Toronto · CAPrincess Margaret Cancer Centre · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Developing therapeutics to effectively inhibit the MYC oncoprotein would mark a key advance towards cancer patient care as MYC is deregulated in over 50% of human cancers. MYC deregulation is correlated with aggressive disease and poor patient outcome. Despite strong evidence in mouse models that inhibiting MYC would significantly impact tumour cell growth and patient survival, traditional approaches have not yet yielded the urgently needed therapeutic agents that directly target MYC. MYC functions through its interaction with MAX to regulate gene transcription by binding to E-box DNA response elements of MYC target genes. Here we used a structure-based strategy to design ME47, a small minimalist hybrid protein (MHP) able to disrupt the MAX:E-box interaction/binding and block transcriptional MYC activity. We show that inducing ME47 expression in established tumour xenografts inhibits tumour growth and decreases cellular proliferation. Mechanistically, we show by chromatin immunoprecipitation that ME47 binds to E-box binding sites of MYC target genes. Moreover, ME47 occupancy decreases MYC:DNA interaction at its cognate E-box binding sites. Taken together, ME47 is a prototypic MHP inhibitor that antagonizes tumour cell growth in vitro and in vivo and inhibits the interaction of MYC with DNA E-box elements. These results support ME47's role as a MYC inhibitor and suggest that MHPs provide an alternative therapeutic targeting system that can be used to target transcription factors important in human diseases, including cancer.

Indexed as

AnimalsBinding, CompetitiveCell Line, TumorChromatin ImmunoprecipitationE-Box ElementsHEK293 CellsHumansMice, Inbred NODMice, SCIDNucleotide MotifsPeptide FragmentsPromoter Regions, GeneticProtein BindingProto-Oncogene Proteins c-mycRecombinant Fusion ProteinsTriple Negative Breast Neoplasmsomomyc proteinPeptide FragmentsProto-Oncogene Proteins c-mycRecombinant Fusion Proteins

Identifiers

PMID28806396
OpenAlexW2746759801

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.