Evidence map›Paper›PMID 31545551›Full record

ArticleMolecular oncology2019

Identification of Eph receptor signaling as a regulator of autophagy and a therapeutic target in colorectal carcinoma.

Michael DiPrima, Dunrui Wang, Alix Tröster, Dragan Maric, Nekane Terrades-Garcia, Taekyu Ha, Hyeongil Kwak, David Sanchez-Martin, Denis Kudlinzki, Harald Schwalbe and 1 more

Abstract read
In one paragraph

Article in Molecular oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Autophagy activation by the Becn1Brain, behavior, and immunity · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Optimization of the Lead Compound NVP-BHG712 as a Colorectal Cancer Inhibitor.Chemistry (Weinheim an der Bergstrasse, Germany) · 2023
    Article
  10. Article
  11. Article
  12. Article
  13. The EPH/Ephrin System in Colorectal Cancer.International journal of molecular sciences · 2022
    Review
  14. Article
  15. A Novel Risk Model Based on Autophagy Pathway Related Genes for Survival Prediction in Lung Adenocarcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  16. Article
  17. 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

11 authors.

Michael DiPrimaLaboratory of Cellular Oncology, Center for Cancer Research (CCR), National Cancer Institute (NCI), Bethesda, MD, USA.
Dunrui WangLaboratory of Cellular Oncology, Center for Cancer Research (CCR), National Cancer Institute (NCI), Bethesda, MD, USA.
Alix TrösterCenter for Biomolecular Magnetic Resonance, Institute for Organic Chemistry and Chemical Biology, Johann Wolfgang Goethe-University, Frankfurt am Main, Germany.
Dragan MaricNational Institutes of Neurological Disorders and Stroke, National Institutes of Health (NIH), Bethesda, MD, USA.
Nekane Terrades-GarciaVasculitis Research Unit, Department of Autoimmune Diseases, Hospital Clinic, University of Barcelona, Spain.
Taekyu HaLaboratory of Cellular Oncology, Center for Cancer Research (CCR), National Cancer Institute (NCI), Bethesda, MD, USA.
Hyeongil KwakLaboratory of Cellular Oncology, Center for Cancer Research (CCR), National Cancer Institute (NCI), Bethesda, MD, USA.
David Sanchez-MartinLaboratory of Cellular Oncology, Center for Cancer Research (CCR), National Cancer Institute (NCI), Bethesda, MD, USA.ORCID 0000-0002-2712-4762
Denis KudlinzkiCenter for Biomolecular Magnetic Resonance, Institute for Organic Chemistry and Chemical Biology, Johann Wolfgang Goethe-University, Frankfurt am Main, Germany.
Harald SchwalbeCenter for Biomolecular Magnetic Resonance, Institute for Organic Chemistry and Chemical Biology, Johann Wolfgang Goethe-University, Frankfurt am Main, Germany.
Giovanna TosatoLaboratory of Cellular Oncology, Center for Cancer Research (CCR), National Cancer Institute (NCI), Bethesda, MD, USA.ORCID 0000-0003-1663-3227

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Advanced colorectal carcinoma is currently incurable, and new therapies are urgently needed. We report that phosphotyrosine-dependent Eph receptor signaling sustains colorectal carcinoma cell survival, thereby uncovering a survival pathway active in colorectal carcinoma cells. We find that genetic and biochemical inhibition of Eph tyrosine kinase activity or depletion of the Eph ligand EphrinB2 reproducibly induces colorectal carcinoma cell death by autophagy. Spautin and 3-methyladenine, inhibitors of early steps in the autophagic pathway, significantly reduce autophagy-mediated cell death that follows inhibition of phosphotyrosine-dependent Eph signaling in colorectal cancer cells. A small-molecule inhibitor of the Eph kinase, NVP-BHG712 or its regioisomer NVP-Iso, reduces human colorectal cancer cell growth in vitro and tumor growth in mice. Colorectal cancers express the EphrinB ligand and its Eph receptors at significantly higher levels than numerous other cancer types, supporting Eph signaling inhibition as a potential new strategy for the broad treatment of colorectal carcinoma.

Indexed as

AutophagyMolecular Targeted TherapySignal TransductionAnimalsCell Line, TumorCell ProliferationCell SurvivalColorectal NeoplasmsEphrin-B2FemaleGene SilencingMiceMice, NudeProtein Kinase InhibitorsPyrazolesPyrimidinesEphrin-B2NVP-BHG712Protein Kinase InhibitorsPyrazolesPyrimidinesReceptors, Eph Familycell deathcolorectal cancerEph receptorsEphrin ligandtyrosine kinase signaling

Identifiers

PMID31545551
PMCPMC6822245

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.