Evidence map›Paper›PMID 26871602›Full record

ArticleOncotarget2016

The mannose receptor LY75 (DEC205/CD205) modulates cellular phenotype and metastatic potential of ovarian cancer cells.

Adnen Faddaoui, Magdalena Bachvarova, Marie Plante, Jean Gregoire, Marie-Claude Renaud, Alexandra Sebastianelli, Stephane Gobeil, Chantale Morin, Elizabeth Macdonald, Barbara Vanderhyden and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. 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
1.9field-weighted citation impact, top 16% 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, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Expression ofTranslational cancer research · 2020
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  10. Systematic Multiomic Analysis ofJournal of clinical medicine · 2020
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  11. Article
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  14. Article
  15. Stories From the Dendritic Cell Guardhouse.Frontiers in immunology · 2019
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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 at 3 institutions in 1 country.

Adnen FaddaouiDepartment of Molecular Medicine, Université Laval, Québec, Canada.
Magdalena BachvarovaCentre de Recherche du CHU de Québec, L'Hôtel-Dieu de Québec, Québec, Canada.
Marie PlanteCentre de Recherche du CHU de Québec, L'Hôtel-Dieu de Québec, Québec, Canada.
Jean GregoireCentre de Recherche du CHU de Québec, L'Hôtel-Dieu de Québec, Québec, Canada.
Marie-Claude RenaudCentre de Recherche du CHU de Québec, L'Hôtel-Dieu de Québec, Québec, Canada.
Alexandra SebastianelliCentre de Recherche du CHU de Québec, L'Hôtel-Dieu de Québec, Québec, Canada.
Stephane GobeilDepartment of Molecular Medicine, Université Laval, Québec, Canada.
Chantale MorinCentre de Recherche du CHU de Québec, L'Hôtel-Dieu de Québec, Québec, Canada.
Elizabeth MacdonaldDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Canada.
Barbara VanderhydenDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Canada.
Dimcho BachvarovDepartment of Molecular Medicine, Université Laval, Québec, Canada.
Université Laval · CAHôtel-Dieu de Québec · CAUniversity of Ottawa · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The molecular basis of epithelial ovarian cancer (EOC) dissemination is still poorly understood. Previously, we identified the mannose receptor LY75 gene as hypomethylated in high-grade (HG) serous EOC tumors, compared to normal ovarian tissues. LY75 represents endocytic receptor expressed on dendritic cells and so far, has been primarily studied for its role in antigen processing and presentation. Here we demonstrate that LY75 is overexpressed in advanced EOC and that LY75 suppression induces mesenchymal-to-epithelial transition (MET) in EOC cell lines with mesenchymal morphology (SKOV3 and TOV112), accompanied by reduction of their migratory and invasive capacity in vitro and enhanced tumor cell colonization and metastatic growth in vivo. LY75 knockdown in SKOV3 cells also resulted in predominant upregulation of functional pathways implicated in cell proliferation and metabolism, while pathways associated with cell signaling and adhesion, complement activation and immune response were mostly suppressed. Moreover, LY75 suppression had an opposite effect on EOC cell lines with epithelial phenotype (A2780s and OV2008), by directing epithelial-to-mesenchymal transition (EMT) associated with reduced capacity for in vivo EOC cell colonization, as similar/identical signaling pathways were reversely regulated, when compared to mesenchymal LY75 knockdown EOC cells.To our knowledge, this is the first report of a gene displaying such pleiotropic effects in sustaining the cellular phenotype of EOC cells and points to novel functions of this receptor in modulating EOC dissemination. Our data also support previous findings regarding the superior capacity of epithelial cancer cells in metastatic colonization of distant sites, compared to cancer cells with mesenchymal-like morphology.

Indexed as

Cell MovementAdultAgedAged, 80 and overAnimalsAntigens, CDApoptosisBiomarkers, TumorCell ProliferationCystadenocarcinoma, SerousEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansLectins, C-TypeMice, Inbred NODAntigens, CDBiomarkers, TumorDEC-205 receptorLectins, C-TypeMinor Histocompatibility AntigensReceptors, Cell SurfaceRNA, Small Interferingepithelial ovarian cancerepithelial-to-mesenchymal transitionintraperitoneal xenograftsLY75 (DEC205)shRNA and CRISPR/Cas9

Identifiers

PMID26871602
PMCPMC4924702
OpenAlexW2259128731

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.