Evidence map›Paper›PMID 35484112›Full record

ArticleSignal transduction and targeted therapy2022

OVOL1 inhibits breast cancer cell invasion by enhancing the degradation of TGF-β type I receptor.

Chuannan Fan, Qian Wang, Gerard van der Zon, Jiang Ren, Cedrick Agaser, Roderick C Slieker, Prasanna Vasudevan Iyengar, Hailiang Mei, Peter Ten Dijke

Open access · goldAbstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.9field-weighted citation impact, top 3% 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

28 citing papers in PubMed, 57 citations in OpenAlex.

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  5. Defining the DNA Binding Specificity of GRHL2.bioRxiv : the preprint server for biology · 2026
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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

9 authors at 1 institution in 1 country.

Chuannan FanDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden, 2300 RC, The Netherlands.ORCID 0000-0001-8754-4913
Qian WangDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden, 2300 RC, The Netherlands.
Gerard van der ZonDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden, 2300 RC, The Netherlands.
Jiang RenDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden, 2300 RC, The Netherlands.
Cedrick AgaserDepartment of Biomedical Data Sciences, Sequencing Analysis Support Core, Leiden University Medical Center, Leiden, 2300 RC, The Netherlands.
Roderick C SliekerDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden, 2300 RC, The Netherlands.ORCID 0000-0003-0961-9152
Prasanna Vasudevan IyengarDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden, 2300 RC, The Netherlands.
Hailiang MeiDepartment of Biomedical Data Sciences, Sequencing Analysis Support Core, Leiden University Medical Center, Leiden, 2300 RC, The Netherlands.
Peter Ten DijkeDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden, 2300 RC, The Netherlands. p.ten_dijke@lumc.nl.
Leiden University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovo-like transcriptional repressor 1 (OVOL1) is a key mediator of epithelial lineage determination and mesenchymal-epithelial transition (MET). The cytokines transforming growth factor-β (TGF-β) and bone morphogenetic proteins (BMP) control the epithelial-mesenchymal plasticity (EMP) of cancer cells, but whether this occurs through interplay with OVOL1 is not known. Here, we show that OVOL1 is inversely correlated with the epithelial-mesenchymal transition (EMT) signature, and is an indicator of a favorable prognosis for breast cancer patients. OVOL1 suppresses EMT, migration, extravasation, and early metastatic events of breast cancer cells. Importantly, BMP strongly promotes the expression of OVOL1, which enhances BMP signaling in turn. This positive feedback loop is established through the inhibition of TGF-β receptor signaling by OVOL1. Mechanistically, OVOL1 interacts with and prevents the ubiquitination and degradation of SMAD family member 7 (SMAD7), which is a negative regulator of TGF-β type I receptor stability. Moreover, a small-molecule compound 6-formylindolo(3,2-b)carbazole (FICZ) was identified to activate OVOL1 expression and thereby antagonizing (at least in part) TGF-β-mediated EMT and migration in breast cancer cells. Our results uncover a novel mechanism by which OVOL1 attenuates TGF-β/SMAD signaling and maintains the epithelial identity of breast cancer cells.

Indexed as

Breast NeoplasmsDNA-Binding ProteinsEpithelial-Mesenchymal TransitionFemaleHumansNeoplasm InvasivenessReceptor, Transforming Growth Factor-beta Type ITranscription FactorsTransforming Growth Factor betaDNA-Binding ProteinsOVOL1 protein, humanReceptor, Transforming Growth Factor-beta Type ITranscription FactorsTransforming Growth Factor beta

Identifiers

PMID35484112
PMCPMC9050647
OpenAlexW4225152006

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.