Evidence map›Paper›PMID 25989290›Full record

ArticleBritish journal of pharmacology2015

The GPR 55 agonist, L-α-lysophosphatidylinositol, mediates ovarian carcinoma cell-induced angiogenesis.

Nicole A Hofmann, Jiang Yang, Sunia A Trauger, Hironao Nakayama, Lan Huang, Dirk Strunk, Marsha A Moses, Michael Klagsbrun, Joyce Bischoff, Wolfgang F Graier

Open access · hybridAbstract read
In one paragraph

Article in British journal of pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-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

25 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  14. Review
  15. Review
  16. Cannabinoids in Gynecological Diseases.Medical cannabis and cannabinoids · 2019
    Review
  17. Article
  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

10 authors at 3 institutions in 3 countries.

Nicole A HofmannInstitute for Molecular Biology and Biochemistry, Medical University Graz, Graz, Austria.
Jiang YangVascular Biology Program, Boston Children's Hospital, Boston, MA, USA.
Sunia A TraugerFAS Small Molecule Mass Spectrometry Facility, Harvard University, Boston, MA, USA.
Hironao NakayamaVascular Biology Program, Boston Children's Hospital, Boston, MA, USA.
Lan HuangVascular Biology Program, Boston Children's Hospital, Boston, MA, USA.
Dirk StrunkExperimental and Clinical Cell Therapy Institute, Paracelsus Medical University, Salzburg, Austria.
Marsha A MosesVascular Biology Program, Boston Children's Hospital, Boston, MA, USA.
Michael KlagsbrunVascular Biology Program, Boston Children's Hospital, Boston, MA, USA.
Joyce BischoffDepartment of Surgery, Harvard Medical School, Boston, MA, USA.
Wolfgang F GraierInstitute for Molecular Biology and Biochemistry, Medical University Graz, Graz, Austria.
Harvard University · USMedical University of Graz · ATParacelsus Medical University · AT

Funding

Austrian Science Fund FWF P 22553Austrian Science Fund FWF W 1226
6 · The paper itself

Abstract

background and purposeHighly vascularized ovarian carcinoma secretes the putative endocannabinoid and GPR55 agonist, L-α-lysophosphatidylinositol (LPI), into the circulation. We aimed to assess the involvement of this agonist and its receptor in ovarian cancer angiogenesis. EXPERIMENTAL APPROACH: Secretion of LPI by three ovarian cancer cell lines (OVCAR-3, OVCAR-5 and COV-362) was tested by mass spectrometry. Involvement of cancer cell-derived LPI on angiogenesis was tested in the in vivo chicken chorioallantoic membrane (CAM) assay along with the assessment of the effect of LPI on proliferation, network formation, and migration of neonatal and adult human endothelial colony-forming cells (ECFCs). Engagement of GPR55 was verified by using its pharmacological inhibitor CID16020046 and diminution of GPR55 expression by four different target-specific siRNAs. To study underlying signal transduction, Western blot analysis was performed. KEY

resultsOvarian carcinoma cell-derived LPI stimulated angiogenesis in the CAM assay. Applied LPI stimulated proliferation, network formation, and migration of neonatal ECFCs in vitro and angiogenesis in the in vivo CAM. The pharmacological GPR55 inhibitor CID16020046 inhibited LPI-stimulated ECFC proliferation, network formation and migration in vitro as well as ovarian carcinoma cell- and LPI-induced angiogenesis in vivo. Four target-specific siRNAs against GPR55 prevented these effects of LPI on angiogenesis. These pro-angiogenic effects of LPI were transduced by GPR55-dependent phosphorylation of ERK1/2 and p38 kinase. CONCLUSIONS AND IMPLICATIONS: We conclude that inhibiting the pro-angiogenic LPI/GPR55 pathway appears a promising target against angiogenesis in ovarian carcinoma.

Indexed as

AnimalsCell Line, TumorCell ProliferationCells, CulturedChickensChorioallantoic MembraneFemaleHumansHuman Umbilical Vein Endothelial CellsLysophospholipidsMAP Kinase Signaling SystemNeovascularization, PathologicOvarian Neoplasmsp38 Mitogen-Activated Protein KinasesReceptors, CannabinoidReceptors, G-Protein-CoupledGPR55 protein, humanlysophosphatidylinositolLysophospholipidsp38 Mitogen-Activated Protein KinasesReceptors, CannabinoidReceptors, G-Protein-Coupled

Identifiers

PMID25989290
PMCPMC4543616
OpenAlexW1745821086

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.