Evidence map›Paper›PMID 29137281›Full record

ArticleOncotarget2017

Hic-5 regulates epithelial to mesenchymal transition in ovarian cancer cells in a TGFβ1-independent manner.

Razan Sheta, Zhi-Qiang Wang, Magdalena Bachvarova, Marie Plante, Jean Gregoire, Marie-Claude Renaud, Alexandra Sebastianelli, Stephane Gobeil, Chantale Morin, Elizabeth Macdonald and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Physiological and pathological roles of Hic‑5 in several organs (Review).International journal of molecular medicine · 2022
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. 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

12 authors at 3 institutions in 1 country.

Razan ShetaDepartment of Molecular Medicine, Université Laval, Québec, Québec, Canada.
Zhi-Qiang WangDepartment of Molecular Medicine, Université Laval, Québec, Québec, Canada.
Magdalena BachvarovaCentre de recherche du CHU de Québec, L'Hôtel-Dieu de Québec, Québec, Québec, Canada.
Marie PlanteCentre de recherche du CHU de Québec, L'Hôtel-Dieu de Québec, Québec, Québec, Canada.
Jean GregoireCentre de recherche du CHU de Québec, L'Hôtel-Dieu de Québec, Québec, Québec, Canada.
Marie-Claude RenaudCentre de recherche du CHU de Québec, L'Hôtel-Dieu de Québec, Québec, Québec, Canada.
Alexandra SebastianelliCentre de recherche du CHU de Québec, L'Hôtel-Dieu de Québec, Québec, Québec, Canada.
Stephane GobeilDepartment of Molecular Medicine, Université Laval, Québec, Québec, Canada.
Chantale MorinCentre de recherche du CHU de Québec, L'Hôtel-Dieu de Québec, Québec, Québec, Canada.
Elizabeth MacdonaldDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario, Canada.
Barbara VanderhydenDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario, Canada.
Dimcho BachvarovDepartment of Molecular Medicine, Université Laval, Québec, Québec, Canada.
Hôtel-Dieu de Québec · CAUniversité Laval · 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. We have previously identified the hydrogen peroxide-inducible clone-5 (Hic-5) gene as hypomethylated in high-grade (HG) serous EOC tumors, compared to normal ovarian tissues. Hic-5 is a focal adhesion scaffold protein and has been primarily studied for its role as a key mediator of TGF-β-induced epithelial-to-mesenchymal transition (EMT) in epithelial cells of both normal and malignant origin; however, its role in EOC has been never investigated. Here we demonstrate that Hic-5 is overexpressed in advanced EOC, and that Hic-5 is upregulated upon TGFβ1 treatment in the EOC cell line with epithelial morphology (A2780s), associated with EMT induction. However, ectopic expression of Hic-5 in A2780s cells induces EMT independently of TGFβ1, accompanied with enhancement of cellular proliferation rate and migratory/invasive capacity and increased resistance to chemotherapeutic drugs. Moreover, Hic-5 knockdown in the EOC cells with mesenchymal morphology (SKOV3) was accompanied by induction of mesenchymal-to-epithelial transition (MET), followed by a reduction of their proliferative, migratory/invasive capacity, and increased drugs sensitivity

Indexed as

epithelial ovarian cancerepithelial-to-mesenchymal transitionHic-5RhoA/ROCKTGFB1I1

Identifiers

PMID29137281
PMCPMC5669907
OpenAlexW2742004115

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.