Evidence map›Paper›PMID 27835572›Full record

ArticleOncotarget2016

Sprouty2 inhibits amphiregulin-induced down-regulation of E-cadherin and cell invasion in human ovarian cancer cells.

Jung-Chien Cheng, Hsun-Ming Chang, Siyuan Xiong, Wai-Kin So, Peter C K Leung

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 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 25% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. The role of amphiregulin in ovarian function and disease.Cellular and molecular life sciences : CMLS · 2023
    Review
  4. Article
  5. Article
  6. Unraveling theFrontiers in pharmacology · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. 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

5 authors at 2 institutions in 1 country.

Jung-Chien ChengDepartment of Obstetrics and Gynaecology, Child & Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada V5Z 4H4.
Hsun-Ming ChangDepartment of Obstetrics and Gynaecology, Child & Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada V5Z 4H4.
Siyuan XiongDepartment of Obstetrics and Gynaecology, Child & Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada V5Z 4H4.
Wai-Kin SoDepartment of Obstetrics and Gynaecology, Child & Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada V5Z 4H4.
Peter C K LeungDepartment of Obstetrics and Gynaecology, Child & Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada V5Z 4H4.
Child and Family Research Institute · CAUniversity of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Similar to Drosophila Sprouty (SPRY), mammalian SPRY proteins inhibit the receptor tyrosine kinase-mediated activation of cellular signaling pathways. SPRY2 expression levels have been shown to be down-regulated in human ovarian cancer, and patients with low SPRY2 expression have significantly poorer survival than those with high SPRY2 expression. In addition, epidermal growth factor receptor (EGFR) is overexpressed in human ovarian cancer and is associated with more aggressive clinical behavior and a poor prognosis. Amphiregulin (AREG), the most abundant EGFR ligand in ovarian cancer, binds exclusively to EGFR and stimulates ovarian cancer cell invasion by down-regulating E-cadherin expression. However, thus far, the roles of SPRY2 in AREG-regulated E-cadherin expression and cell invasion remain unclear. In the present study, we show that treatment with AREG up-regulated SPRY2 expression by activating the EGFR-mediated ERK1/2 signaling pathway in two human ovarian cancer cell lines, SKOV3 and OVCAR5. In addition, overexpression of SPRY2 attenuated the AREG-induced down-regulation of E-cadherin by inhibiting the induction of the E-cadherin transcriptional repressor, Snail. Moreover, SPRY2 overexpression attenuated AREG-stimulated cell invasion and proliferation. This study reveals that SPRY2 acts as a tumor suppressor in human ovarian cancer and illustrates the underlying mechanisms that can be used as possible targets for the development of novel therapeutics.

Indexed as

Cell MovementAmphiregulinAntigens, CDAntineoplastic AgentsCadherinsCell Line, TumorCell ProliferationDisease-Free SurvivalErbB ReceptorsExtracellular Signal-Regulated MAP KinasesFemaleGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsKaplan-Meier EstimateLigandsAmphiregulinAntigens, CDAntineoplastic AgentsAREG protein, humanCadherinsCDH1 protein, humanEGFR protein, humanErbB ReceptorsExtracellular Signal-Regulated MAP KinasesIntracellular Signaling Peptides and ProteinsLigandsMembrane ProteinsQuinazolinesRTKI cpdSnail Family Transcription FactorsSPRY2 protein, humanTyrphostinsamphiregulinE-cadherinovarian cancersprouty2

Identifiers

PMID27835572
PMCPMC5348419
OpenAlexW2554128115

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.