Evidence map›Paper›PMID 27195958›Full record

ArticlePloS one2016

WNT7A Regulation by miR-15b in Ovarian Cancer.

James A MacLean, Mandy L King, Hiroshi Okuda, Kanako Hayashi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Mechanistic Insights into Tumorigenesis from Serum Proteins.medRxiv : the preprint server for health sciences · 2025
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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

4 authors at 2 institutions in 2 countries.

James A MacLeanDepartment of Physiology, Southern Illinois University School of Medicine, Carbondale, Illinois, United States of America.
Mandy L KingDepartment of Physiology, Southern Illinois University School of Medicine, Carbondale, Illinois, United States of America.
Hiroshi OkudaLaboratory for Malignancy Control Research, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Kanako HayashiDepartment of Physiology, Southern Illinois University School of Medicine, Carbondale, Illinois, United States of America.ORCID 0000-0002-5028-799X
Southern Illinois University School of Medicine · USKyoto University · JP

Funding

Mechanisms of WNT7A-FGF1 signaling and their therapeutic potential in ovarian canR15CA179214 · NCI · SOUTHERN ILLINOIS UNIVERSITY CARBONDALE · PI HAYASHI, KANAKO · 2013 to 2013
$443k
NCI NIH HHS R15 CA179214
6 · The paper itself

Abstract

WNT signaling is well known to play an important role in the regulation of development, cell proliferation and cell differentiation in a wide variety of normal and cancerous tissues. Despite the wealth of knowledge concerning when and where various WNT genes are expressed and downstream events under their control, there is surprisingly little published evidence of how they are regulated. We have recently reported that aberrant WNT7A is observed in serous ovarian carcinomas, and WNT7A is the sole ligand accelerating ovarian tumor progression through CTNNB1 (β-catenin)/TCF signaling in the absence of CTNNB1 mutations. In the present study, we report that WNT7A is a direct target of miR-15b in ovarian cancer. We showed that a luciferase reporter containing the putative binding site of miR-15b in the WNT7A 3'-UTR was significantly repressed by miR-15b. Mutation of the putative binding site of miR-15b in the WNT7A 3'-UTR restored luciferase activity. Furthermore, miR-15b was able to repress increased levels of TOPFLASH activity by WNT7A, but not those induced by S33Y. Additionally, miR-15b dose-dependently decreased WNT7A expression. When we evaluated the prognostic impact of WNT7A and miR-15b expression using TCGA datasets, a significant inverse correlation in which high-expression of WNT7A and low-expression of miR-15b was associated with reduced survival rates of ovarian cancer patients. Treatment with decitabine dose-dependently increased miR-15b expression, and silencing of DNMT1 significantly increased miR-15b expression. These results suggest that WNT7A is post-transcriptionally regulated by miR-15b, which could be down-regulated by promoter hypermethylation, potentially via DNMT1, in ovarian cancer.

Indexed as

3' Untranslated RegionsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMicroRNAsMutationOvarian NeoplasmsWnt Proteins3' Untranslated RegionsMicroRNAsMIRN15 microRNA, humanWNT7A protein, humanWnt Proteins

Identifiers

PMID27195958
PMCPMC4873135
OpenAlexW2397092993

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.