Evidence map›Paper›PMID 31748508›Full record

ArticleExperimental & molecular medicine2019

VGLL4 interacts with STAT3 to function as a tumor suppressor in triple-negative breast cancer.

Hongming Song, Qifeng Luo, Xiaochong Deng, Changle Ji, Dengfeng Li, Amik Munankarmy, Wei Jian, Junyong Zhao, Lin Fang

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 16% 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, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

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  20. MaternalFrontiers in cell and developmental biology · 2024
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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

9 authors at 3 institutions in 1 country.

Hongming Song *Department of Breast and Thyroid Surgery, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, 200072, Shanghai, China.
Qifeng LuoDepartment of Breast and Thyroid Surgery, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, 200072, Shanghai, China.
Xiaochong DengDepartment of Breast and Thyroid Surgery, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, 200072, Shanghai, China.
Changle JiDepartment of Breast and Thyroid Surgery, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, 200072, Shanghai, China.
Dengfeng LiDepartment of Breast and Thyroid Surgery, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, 200072, Shanghai, China.
Amik MunankarmyDepartment of Breast and Thyroid Surgery, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, 200072, Shanghai, China.
Wei JianDepartment of Breast and Thyroid Surgery, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, 200072, Shanghai, China.
Junyong ZhaoDepartment of Breast and Thyroid Surgery, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, 200072, Shanghai, China.
Lin FangDepartment of Breast and Thyroid Surgery, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, 200072, Shanghai, China. fanglin2017@126.com.
Tongji University · CNAffiliated Hospital of Qingdao University · CNShanghai Tenth People's Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82172240Shanghai Municipal Health Bureau (Shanghai Municipal Public Health Bureau) 201640097
6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) is an aggressive malignancy with a poor prognosis, and there are no effective molecular-targeted drugs for TNBC patients in clinical practice. The JAK-STAT pathway is implicated in tumorigenesis and the progression of various cancers. In this study, the results demonstrated that VGLL4 is expressed at low levels in both TNBC specimens and cell lines and that VGLL4 expression is negatively correlated with Ki67 expression and tumor size in TNBC patients. VGLL4 knockdown can promote the growth of TNBC cells, while VGLL4 overexpression significantly suppresses the growth of TNBC cells in vitro. More importantly, VGLL4 significantly inhibits tumor progression in a nude mouse model. In addition, VGLL4 is a direct target of miR-454, and the upregulation of miR-454 decreases VGLL4 expression and promotes the cell growth of TNBC cells. Furthermore, we also demonstrated that VGLL4 interacts with STAT3, the core component of the JAK-STAT pathway, leading to the inactivation of STAT3 and the inhibition of STAT3 downstream transcription. Collectively, these findings indicate that VGLL4 expression is negatively associated with poor prognosis in TNBC patients. High expression of miR-454 may be one of the causes of the downregulation of VGLL4 in TNBC, and VGLL4 acts as a tumor suppressor in TNBC by interacting with STAT3 and subsequently suppresses the STAT3 signaling axis, providing potential biomarkers and therapeutic approaches for this fatal disease.

Indexed as

AnimalsCell Line, TumorCell MovementCell ProliferationFemaleFlow CytometryGene Expression Regulation, NeoplasticHumansImmunoprecipitationMiceProtein BindingSignal TransductionSTAT3 Transcription FactorTranscription FactorsTriple Negative Breast NeoplasmsXenograft Model Antitumor AssaysSTAT3 protein, humanSTAT3 Transcription FactorTranscription FactorsVGLL4 protein, human

Identifiers

PMID31748508
PMCPMC6868227
OpenAlexW2990526911

What OpenQuestion holds

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LicenceCC BY
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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.