Evidence map›Paper›PMID 42050622›Full record

ArticleJournal of translational medicine2026

FAT4 restrains epithelial-mesenchymal transition and metastasis in cervical cancer and shapes the tumor immune microenvironment.

Dongying Wang, Shuying Wu, Hongxin Wang, Beijia Yan, Yuxuan Zhang, Jiaxing He, Tianmin Xu

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PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

7 authors.

Dongying WangObstetrics and Gynecology Department, The Second Hospital of Jilin University, 4026 Ya Tai Street, Changchun, Jilin, 130041, China.ORCID 0000-0001-9881-8596
Shuying WuObstetrics and Gynecology Department, The Second Hospital of Jilin University, 4026 Ya Tai Street, Changchun, Jilin, 130041, China.
Hongxin WangObstetrics and Gynecology Department, The Second Hospital of Jilin University, 4026 Ya Tai Street, Changchun, Jilin, 130041, China.
Beijia YanObstetrics and Gynecology Department, The Second Hospital of Jilin University, 4026 Ya Tai Street, Changchun, Jilin, 130041, China.
Yuxuan ZhangDepartment of Tumor Radiotherapy, The Second Hospital of Jilin University, 4026 Ya Tai Street, Changchun, Jilin, 130041, China.
Jiaxing HeObstetrics and Gynecology Department, The Second Hospital of Jilin University, 4026 Ya Tai Street, Changchun, Jilin, 130041, China.
Tianmin XuObstetrics and Gynecology Department, The Second Hospital of Jilin University, 4026 Ya Tai Street, Changchun, Jilin, 130041, China. xutianmin@126.com.ORCID 0000-0002-1219-061X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMetastatic dissemination remains the major cause of mortality in cervical cancer. FAT4, an atypical cadherin upstream of Hippo signaling, has been implicated in tumor suppression, yet its clinical relevance and mechanistic role in cervical cancer metastasis are insufficiently defined.

methodsWe assessed FAT4 expression by immunohistochemistry in 40 paired cervical cancer and adjacent tissues and analyzed clinicopathological associations. The immune landscape of 10 freshly resected tumors was profiled using mass cytometry (CyTOF). To interrogate causality, we activated endogenous FAT4 using CRISPR activation (dCas9-SAM) in cervical cancer cell lines, followed by migration/invasion assays and EMT marker analyses. Metastatic potential was evaluated in xenograft and syngeneic mouse models.

resultsFAT4 expression was reduced in tumors compared with matched non-tumor tissues and aligned with metastatic features. CyTOF delineated distinct immune compositions between FAT4-high and FAT4-low tumors, indicating a remodeled tumor immune microenvironment. CRISPRa-mediated FAT4 activation curtailed cell migration and invasion, restored epithelial markers, and suppressed mesenchymal markers, consistent with epithelial-mesenchymal transition (EMT) restraint. In vivo, enforced FAT4 reduced metastatic burden. Mechanistically, FAT4 activation was associated with suppression of EMT transcriptional programs and with signaling signatures consistent with reduced PI3K–AKT/Wnt/Hippo pathway signatures.

conclusionsFAT4 acts as a metastasis suppressor in cervical cancer by constraining EMT and remodeling the tumor immune microenvironment. These data support FAT4 as a potential biomarker and therapeutic entry point for metastasis control.

Indexed as

CadherinsEpithelial-Mesenchymal TransitionTumor MicroenvironmentUterine Cervical NeoplasmsAnimalsCell Line, TumorCell MovementFemaleHumansMiceNeoplasm InvasivenessNeoplasm MetastasisSignal TransductionTumor Suppressor ProteinsCadherinsFAT4 protein, humanTumor Suppressor ProteinsCervical cancerCyTOFEpithelial–mesenchymal transitionFAT4MetastasisTumor microenvironment

Identifiers

PMID42050622
PMCPMC13156880

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.