Evidence map›Paper›PMID 33999334›Full record

ReviewMolecular and cellular biochemistry2021

Wnt/β-catenin signaling pathway in uterine leiomyoma: role in tumor biology and targeting opportunities.

Malak El Sabeh, Subbroto Kumar Saha, Sadia Afrin, Md Soriful Islam, Mostafa A Borahay

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Molecular and cellular biochemistry, 2021. 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
4.1field-weighted citation impact, top 5% 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, 50 citations in OpenAlex.

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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 1 institution in 1 country.

Malak El Sabeh *Department of Gynecology & Obstetrics, Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Subbroto Kumar Saha *Department of Gynecology & Obstetrics, Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Sadia AfrinDepartment of Gynecology & Obstetrics, Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Md Soriful IslamDepartment of Gynecology & Obstetrics, Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD, 21205, USA.
Mostafa A BorahayDepartment of Gynecology & Obstetrics, Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD, 21205, USA. mboraha1@jhmi.edu.ORCID http://orcid.org/0000-0002-0554-132X
Johns Hopkins University · US

Funding

Mechanisms of actions(s) of simvastatin in uterine leiomyomaR01HD094380 · NICHD · JOHNS HOPKINS UNIVERSITY · PI BORAHAY, MOSTAFA A. · 2018 to 2022
$4.0M
Eunice Kennedy Shriver National Institute of Child Health and Human Development 1R01HD094380NICHD NIH HHS R01 HD094380
6 · The paper itself

Abstract

Uterine leiomyoma is the most common tumor of the female reproductive system and originates from a single transformed myometrial smooth muscle cell. Despite the immense medical, psychosocial, and financial impact, the exact underlying mechanisms of leiomyoma pathobiology are poorly understood. Alterations of signaling pathways are thought to be instrumental in leiomyoma biology. Wnt/β-catenin pathway appears to be involved in several aspects of the genesis of leiomyomas. For example, Wnt5b is overexpressed in leiomyoma, and the Wnt/β-catenin pathway appears to mediate the role of MED12 mutations, the most common mutations in leiomyoma, in tumorigenesis. Moreover, Wnt/β-catenin pathway plays a paracrine role where estrogen/progesterone treatment of mature myometrial or leiomyoma cells leads to increased expression of Wnt11 and Wnt16, which induces proliferation of leiomyoma stem cells and tumor growth. Constitutive activation of β-catenin leads to myometrial hyperplasia and leiomyoma-like lesions in animal models. Wnt/β-catenin signaling is also closely involved in mechanotransduction and extracellular matrix regulation and relevant alterations in leiomyoma, and crosstalk is noted between Wnt/β-catenin signaling and other pathways known to regulate leiomyoma development and growth such as estrogen, progesterone, TGFβ, PI3K/Akt/mTOR, Ras/Raf/MEK/ERK, IGF, Hippo, and Notch signaling. Finally, evidence suggests that inhibition of the canonical Wnt pathway using β-catenin inhibitors inhibits leiomyoma cell proliferation. Understanding the molecular mechanisms of leiomyoma development is essential for effective treatment. The specific Wnt/β-catenin pathway molecules discussed in this review constitute compelling candidates for therapeutic targeting.

Indexed as

Molecular Targeted TherapyAnimalsAntineoplastic AgentsFemaleHumansLeiomyomaUterine NeoplasmsWnt Signaling PathwayAntineoplastic AgentsLeiomyomaPathobiologySignaling pathwayUterine fibroidWnt/β-catenin pathway

Identifiers

PMID33999334
PMCPMC9235413
OpenAlexW3161719572

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Registered trials

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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.