Evidence map›Paper›PMID 38334836›Full record

ReviewCellular and molecular life sciences : CMLS2024

Wnt/β-catenin-driven EMT regulation in human cancers.

Wenhua Xue, Lin Yang, Chengxin Chen, Milad Ashrafizadeh, Yu Tian, Ranran Sun

Expression of concernOpen access · goldAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 216 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
216citing papers in PubMed, 3 pooled it
59.6field-weighted citation impact, top 1% 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

216 citing papers in PubMed, 3 syntheses or guidelines pooled it, 255 citations in OpenAlex.

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  14. Multi-omic Profiling of Recurrence Risk Across Breast Cancer Subtypes.medRxiv : the preprint server for health sciences · 2026
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156 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

Wenhua Xue *Department of Pharmacy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, People's Republic of China.
Lin Yang *Department of Hepatobiliary Surgery, Xianyang Central Hospital, Xianyang, 712000, Shaanxi, China.
Chengxin ChenDepartment of Pharmacy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, People's Republic of China.
Milad AshrafizadehShanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, 200032, China. dvm.milad1994@gmail.com.ORCID http://orcid.org/0000-0001-6605-822X
Yu TianSchool of Public Health, Benedictine University, Lisle, USA. Tian_Yu@ben.edu.
Ranran SunPrecision Medicine Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. fccsunrr@zzu.edu.cn.
First Affiliated Hospital of Zhengzhou University · CNBenedictine University · USSun Yat-sen University · CNXian Yang Central Hospital · CN

Funding

Medical Science and Technology Project of Henan Province SBGJ202002077Natural Science Foundation of Henan Province of China 202300410460Young and Middle-aged Health Science and Technology Innovation Talents in 2020 YXKC2020055
6 · The paper itself

Abstract

Metastasis accounts for 90% of cancer-related deaths among the patients. The transformation of epithelial cells into mesenchymal cells with molecular alterations can occur during epithelial-mesenchymal transition (EMT). The EMT mechanism accelerates the cancer metastasis and drug resistance ability in human cancers. Among the different regulators of EMT, Wnt/β-catenin axis has been emerged as a versatile modulator. Wnt is in active form in physiological condition due to the function of GSK-3β that destructs β-catenin, while ligand-receptor interaction impairs GSK-3β function to increase β-catenin stability and promote its nuclear transfer. Regarding the oncogenic function of Wnt/β-catenin, its upregulation occurs in human cancers and it can accelerate EMT-mediated metastasis and drug resistance. The stimulation of Wnt by binding Wnt ligands into Frizzled receptors can enhance β-catenin accumulation in cytoplasm that stimulates EMT and related genes upon nuclear translocation. Wnt/β-catenin/EMT axis has been implicated in augmenting metastasis of both solid and hematological tumors. The Wnt/EMT-mediated cancer metastasis promotes the malignant behavior of tumor cells, causing therapy resistance. The Wnt/β-catenin/EMT axis can be modulated by upstream mediators in which non-coding RNAs are main regulators. Moreover, pharmacological intervention, mainly using phytochemicals, suppresses Wnt/EMT axis in metastasis suppression.

Indexed as

beta CateninNeoplasmsCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3 betaHumansWnt Signaling Pathwaybeta CateninGlycogen Synthase Kinase 3 betaCancer metastasisChemoresistanceEMTPhytochemicalsWnt/β-catenin

Identifiers

PMID38334836
PMCPMC10857981
OpenAlexW4391691695

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.