Evidence map›Paper›PMID 41882663›Full record

ArticleBiology direct2026

FAM83D facilitates EMT and metastasis of cervical cancer via interaction with GSK3β and inactivation of GSK3β/stabilization of Snail signaling.

Jiaofeng Li, Fengtian Li, Xia Meng, Zhiling Yang, Zhengguang Li, Hualong Tang, Wanglong Zhu, Haoming Li, Xingqiang He, Xinyue Lin and 5 more

Abstract read
In one paragraph

Article in Biology direct, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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

15 authors.

Jiaofeng Li *The Second Affiliated Hospital of Chengdu Medical College, China National Nuclear Corporation 416 Hospital, Chengdu, 61051, China.
Fengtian Li *The Second Affiliated Hospital of Chengdu Medical College, China National Nuclear Corporation 416 Hospital, Chengdu, 61051, China.
Xia Meng *The Second Affiliated Hospital of Chengdu Medical College, China National Nuclear Corporation 416 Hospital, Chengdu, 61051, China.
Zhiling Yang *The Second Affiliated Hospital of Chengdu Medical College, China National Nuclear Corporation 416 Hospital, Chengdu, 61051, China.
Zhengguang LiThe Affiliated Cancer Hospital of Chengdu Medical College, Oncology Department of Chengdu Seventh People's Hospital, Chengdu, 610213, China.
Hualong TangSchool of Bioscience and Technology, Chengdu Medical College, Chengdu, 610500, China.
Wanglong ZhuSchool of Bioscience and Technology, Chengdu Medical College, Chengdu, 610500, China.
Haoming LiSchool of Bioscience and Technology, Chengdu Medical College, Chengdu, 610500, China.
Xingqiang HeSchool of Bioscience and Technology, Chengdu Medical College, Chengdu, 610500, China.
Xinyue LinSchool of Bioscience and Technology, Chengdu Medical College, Chengdu, 610500, China.
Zhengyu HanSchool of Bioscience and Technology, Chengdu Medical College, Chengdu, 610500, China.
Mei ChenSchool of Bioscience and Technology, Chengdu Medical College, Chengdu, 610500, China.
Yuhan YangThe Second Affiliated Hospital of Chengdu Medical College, China National Nuclear Corporation 416 Hospital, Chengdu, 61051, China. yangyuhan@cmc.edu.cn.
Jingyi WangThe Second Affiliated Hospital of Chengdu Medical College, China National Nuclear Corporation 416 Hospital, Chengdu, 61051, China. wjy416h@163.com.
Kun ZhangThe Second Affiliated Hospital of Chengdu Medical College, China National Nuclear Corporation 416 Hospital, Chengdu, 61051, China. zhangkunyyo@cmc.edu.cn.

Funding

Clinical Science Research Foundations of Collaborative Innovation Center of Sichuan for Elderly Care and Health 2022LHTD-02CMC Excellent-talent Program 2024kjTzn03Development and Regeneration Key Lab of Sichuan Province 24LHFYSZ1-27National Natural Science Foundation of China 82272658 and 81872451Organized Research Projects of Chengdu Medical College CYYZZ24-01Sichuan Higher Education Institute Key Laboratory of Major Disease Target Discovery and Protein Drug Development 23LHNBZZD07, 24LHBBYY1-08, 24LHBBYY1-09Sichuan Science and Technology Program 2022JDRC0042 and 2022NSFSC0777
6 · The paper itself

Abstract

FAM83D plays a crucial role in cervical cancer (CC) metastasis, though its exact mechanism remains unclear. This study found that FAM83D was significantly upregulated in CC tissues, particularly in metastatic cases, and correlated with advanced tumor stage and poor prognosis. While it did not affect CC cell proliferation, chemosensitivity, or tumorigenesis, FAM83D overexpression enhanced migration and invasion, whereas its knockdown suppressed these effects. In vivo, silencing FAM83D markedly reduced lung and liver metastases in mice. Mechanistically, FAM83D upregulated EMT-like changes and Snail stability by directly interacting with GSK3β and promoting its Ser9 phosphorylation, thereby activating GSK3β/Snail signaling. Furthermore, AKT and PKA served as key upstream kinases in FAM83D-mediated GSK3β inactivation. Inhibition of GSK3β reversed the anti-metastatic effects of FAM83D knockdown. These results identify FAM83D as a key metastasis driver in CC, functioning through GSK3β/Snail/EMT axis, and suggest its potential as a therapeutic target to inhibit CC progression.

Indexed as

Cell Cycle ProteinsEpithelial-Mesenchymal TransitionGlycogen Synthase Kinase 3 betaSnail Family Transcription FactorsUterine Cervical NeoplasmsAnimalsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMiceMicrotubule-Associated ProteinsNeoplasm MetastasisSignal TransductionCell Cycle ProteinsFAM83D protein, humanGlycogen Synthase Kinase 3 betaGSK3B protein, humanMicrotubule-Associated ProteinsSnail Family Transcription FactorsCervical cancerEMTFAM83DMetastasis

Identifiers

PMID41882663
PMCPMC13137487

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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.