Evidence map›Paper›PMID 34510826›Full record

ArticleFEBS open bio2021

Reduced MAGI3 level by HPV18E6 contributes to Wnt/β-catenin signaling activation and cervical cancer progression.

Zhuoli Yang, Hua Liu, Ran Song, Wenxiu Lu, Haibo Wang, Siyu Gu, Xuedi Cao, Yibin Chen, Jihuan Liang, Qiong Qin and 3 more

Open access · goldAbstract read
In one paragraph

Article in FEBS open bio, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 33% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
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  4. Review
  5. YTHDC1-Mediated mJournal of agricultural and food chemistry · 2026
    Article
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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

13 authors at 2 institutions in 1 country.

Zhuoli YangDepartment of Biochemistry and Molecular Biology, Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University, Beijing, China.
Hua LiuDepartment of Biochemistry and Molecular Biology, Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University, Beijing, China.
Ran SongDepartment of Biochemistry and Molecular Biology, Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University, Beijing, China.
Wenxiu LuDepartment of Biochemistry and Molecular Biology, Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University, Beijing, China.
Haibo WangDepartment of Biochemistry and Molecular Biology, Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University, Beijing, China.
Siyu GuDepartment of Biochemistry and Molecular Biology, Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University, Beijing, China.
Xuedi CaoDepartment of Biochemistry and Molecular Biology, Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University, Beijing, China.
Yibin ChenDepartment of Biochemistry and Molecular Biology, Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University, Beijing, China.
Jihuan LiangDepartment of Biochemistry and Molecular Biology, Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University, Beijing, China.
Qiong QinDepartment of Biochemistry and Molecular Biology, Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University, Beijing, China.
Xiaomei YangDepartment of Biochemistry and Molecular Biology, Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University, Beijing, China.
Duiping FengDepartment of Interventional Radiology, First Hospital of Shanxi Medical University, Taiyuan, China.
Junqi HeDepartment of Biochemistry and Molecular Biology, Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University, Beijing, China.ORCID 0000-0002-5921-1297
Capital Medical University · CNShanxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human papillomavirus type 18 (HPV18) has high carcinogenic power in invasive cervical cancer (ICC) development. However, the underlying mechanism remains elusive. The carcinogenic properties of HPV18 require the PDZ-binding motif of its E6 oncoprotein (HPV18 E6) to degrade its target PSD95/Dlg/ZO-1 (PDZ) proteins. In this study, we demonstrated that the PDZ protein membrane-associated guanylate kinase, WW and PDZ domain containing 3 (MAGI3) inhibited the Wnt/β-catenin pathway, and subsequently cervical cancer (CC) cell migration and invasion, via decreasing β-catenin levels. By reducing MAGI3 protein levels, HPV18 E6 promoted CC cell migration and invasion through activation of Wnt/β-catenin signaling. Furthermore, HPV18 rather than HPV16 was preferentially associated with the downregulation of MAGI3 and activation of the Wnt/β-catenin pathway in CC. These findings shed light on the mechanism that gives HPV18 its high carcinogenic potential in CC progression.

Indexed as

Adaptor Proteins, Signal Transducingbeta CateninCell Line, TumorCell MovementChinaFemaleGene Expression Regulation, NeoplasticHuman papillomavirus 18HumansMembrane ProteinsNeoplasm InvasivenessOncogene Proteins, ViralPapillomavirus InfectionsRepressor ProteinsTranscription FactorsUterine Cervical NeoplasmsAdaptor Proteins, Signal Transducingbeta CateninMAGI3 protein, humanMembrane ProteinsOncogene Proteins, ViralRepressor ProteinsTranscription Factorscervical cancerHPVinvasionMAGI3PDZWnt/β-catenin

Identifiers

PMID34510826
PMCPMC8564337
OpenAlexW3199064876

What OpenQuestion holds

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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.