Evidence map›Paper›PMID 29713059›Full record

ArticleOncogene2018

Inactivation of the serine protease HTRA1 inhibits tumor growth by deregulating angiogenesis.

Ralph Klose, M Gordian Adam, Eva-Maria Weis, Iris Moll, Joycelyn Wüstehube-Lausch, Fabian Tetzlaff, Chio Oka, Michael Ehrmann, Andreas Fischer

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  5. Progress to Clarify HowBiomolecules · 2024
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  8. Notch Signaling in the Vasculature: Angiogenesis and Angiocrine Functions.Cold Spring Harbor perspectives in medicine · 2023
    Review
  9. Current Views on Chr10q26 Contribution to Age-Related Macular Degeneration.Advances in experimental medicine and biology · 2023
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
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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

9 authors at 3 institutions in 2 countries.

Ralph KloseDivision Vascular Signaling and Cancer (A270), German Cancer Research Center, Heidelberg, 69120, Germany.
M Gordian AdamDivision Vascular Signaling and Cancer (A270), German Cancer Research Center, Heidelberg, 69120, Germany.
Eva-Maria WeisDivision Vascular Signaling and Cancer (A270), German Cancer Research Center, Heidelberg, 69120, Germany.
Iris MollDivision Vascular Signaling and Cancer (A270), German Cancer Research Center, Heidelberg, 69120, Germany.
Joycelyn Wüstehube-LauschDivision Vascular Signaling and Cancer (A270), German Cancer Research Center, Heidelberg, 69120, Germany.
Fabian TetzlaffDivision Vascular Signaling and Cancer (A270), German Cancer Research Center, Heidelberg, 69120, Germany.
Chio OkaLaboratory of Gene Function in Animals, Nara Institute of Science and Technology, 8916-5 Takayama, Ikoma, Nara, 630-0192, Japan.
Michael EhrmannCentre of Medical Biotechnology, Faculty of Biology, University Duisburg-Essen, Essen, 45117, Germany.ORCID http://orcid.org/0000-0002-1927-260X
Andreas FischerDivision Vascular Signaling and Cancer (A270), German Cancer Research Center, Heidelberg, 69120, Germany. a.fischer@dkfz.de.ORCID http://orcid.org/0000-0002-4889-0909
German Cancer Research Center · DENara Institute of Science and Technology · JPUniversity of Duisburg-Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The serine protease HTRA1 is involved in several vascular diseases and its expression is often deregulated in cancer. We aimed at identifying how HTRA1 in the vasculature affects tumor growth. Here we report that silencing of HTRA1 in cultured endothelial cells increased migration rate and tube formation, whereas forced HTRA1 expression impaired sprouting angiogenesis. Mechanistically, endothelial HTRA1 expression enhanced Delta/Notch signaling by reducing the amount of the weak Notch ligand JAG1. HTRA1 physically interacted with JAG1 and cleaved it within the intracellular domain, leading to protein degradation. Expression of a constitutive active Notch1 prevented the hypersprouting phenotype upon silencing of HTRA1. In HtrA1-deficient mice, endothelial Notch signaling was diminished and isolated endothelial cells had increased expression of VEGF receptor-2. Growth of syngeneic tumors was strongly impaired in HtrA1

Indexed as

AnimalsCell Line, TumorCell MovementCell ProliferationCells, CulturedHigh-Temperature Requirement A Serine Peptidase 1HumansHuman Umbilical Vein Endothelial CellsIntracellular Signaling Peptides and ProteinsJagged-1 ProteinMelanoma, ExperimentalMembrane ProteinsMiceMice, Inbred C57BLNeoplasmsNeovascularization, Pathologicdelta proteinHigh-Temperature Requirement A Serine Peptidase 1HtrA1 protein, mouseIntracellular Signaling Peptides and ProteinsJagged-1 ProteinMembrane ProteinsReceptors, NotchVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID29713059
OpenAlexW2800586186

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.