Evidence map›Paper›PMID 30194764›Full record

ArticleInternational journal of cancer2019

PDEδ inhibition impedes the proliferation and survival of human colorectal cancer cell lines harboring oncogenic KRas.

Christian H Klein, Dina C Truxius, Holger A Vogel, Jana Harizanova, Sandip Murarka, Pablo Martín-Gago, Philippe I H Bastiaens

Open access · hybridAbstract read
In one paragraph

Article in International journal of cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
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  7. RAS degraders: The new frontier for RAS-driven cancers.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Review
  8. Article
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  10. Development of PD3 and PD3-B for PDEδ inhibition to modulate KRAS activity.Journal of enzyme inhibition and medicinal chemistry · 2022
    Article
  11. Article
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  13. Review
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  18. Understanding Ras Spatial Cycles Through Reaction-Diffusion Simulations.Methods in molecular biology (Clifton, N.J.) · 2021
    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

7 authors at 2 institutions in 1 country.

Christian H KleinDepartment of Systemic Cell Biology, Max Planck Institute for Molecular Physiology, Dortmund, Germany.
Dina C TruxiusDepartment of Systemic Cell Biology, Max Planck Institute for Molecular Physiology, Dortmund, Germany.
Holger A VogelDepartment of Systemic Cell Biology, Max Planck Institute for Molecular Physiology, Dortmund, Germany.
Jana HarizanovaDepartment of Systemic Cell Biology, Max Planck Institute for Molecular Physiology, Dortmund, Germany.
Sandip MurarkaDepartment of Chemical Biology, Max Planck Institute for Molecular Physiology, Dortmund, Germany.
Pablo Martín-GagoDepartment of Chemical Biology, Max Planck Institute for Molecular Physiology, Dortmund, Germany.
Philippe I H BastiaensDepartment of Systemic Cell Biology, Max Planck Institute for Molecular Physiology, Dortmund, Germany.ORCID 0000-0001-8873-6909
Max Planck Institute of Molecular Physiology · DETU Dortmund University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ras proteins, most notably KRas, are prevalent oncogenes in human cancer. Plasma membrane localization and thereby signaling of KRas is regulated by the prenyl-binding protein PDEδ. Recently, we have reported the specific anti-proliferative effects of PDEδ inhibition in KRas-dependent human pancreatic ductal adenocarcinoma cell lines. Here, we investigated the proliferative dependence on the solubilizing activity of PDEδ of human colorectal cancer (CRC) cell lines with or without oncogenic KRas mutations. Our results show that genetic and pharmacologic interference with PDEδ specifically inhibits proliferation and survival of CRC cell lines harboring oncogenic KRas mutations whereas isogenic cell lines in which the KRas oncogene has been removed, or cell lines with oncogenic BRaf mutations or EGFR overexpression are not dependent on PDEδ. Pharmacological PDEδ inhibition is therefore a possible new avenue to target oncogenic KRas bearing CRC.

Indexed as

ApoptosisBenzimidazolesCell Line, TumorCell ProliferationCell SurvivalColorectal NeoplasmsCyclic Nucleotide Phosphodiesterases, Type 6Gene Expression Regulation, NeoplasticHCT116 CellsHT29 CellsHumansMutationProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)RNA InterferenceBenzimidazolesCyclic Nucleotide Phosphodiesterases, Type 6deltarasinKRAS protein, humanProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)colorectal cancerKRasPDEδproliferation

Identifiers

PMID30194764
PMCPMC6519276
OpenAlexW2950267096

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.