Evidence map›Paper›PMID 35109842›Full record

ArticleCancer cell international2022

DNMT1 facilitates growth of breast cancer by inducing MEG3 hyper-methylation.

Xiaotao Zhu, Lin Lv, Mingzheng Wang, Chen Fan, Xiaofeng Lu, Miaomiao Jin, Shuguang Li, Fan Wang

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

21 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  5. Harnessing the Role ofInternational journal of molecular sciences · 2025
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  6. The breast journal · 2025
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  10. Medicina (Kaunas, Lithuania) · 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

8 authors at 1 institution in 1 country.

Xiaotao ZhuDepartment of Thyroid Breast Surgery, Jinhua Municipal Central Hospital, No. 365 East Renmin Road, Jinhua, 321000, Zhejiang, China.
Lin LvDepartment of Thyroid Breast Surgery, Jinhua Municipal Central Hospital, No. 365 East Renmin Road, Jinhua, 321000, Zhejiang, China.
Mingzheng WangDepartment of Thyroid Breast Surgery, Jinhua Municipal Central Hospital, No. 365 East Renmin Road, Jinhua, 321000, Zhejiang, China.
Chen FanDepartment of Breast Surgery, Women and Children Branch of Jinhua Municipal Central Hospital, Jinhua, 321000, China.
Xiaofeng LuDepartment of Thyroid Breast Surgery, Jinhua Municipal Central Hospital, No. 365 East Renmin Road, Jinhua, 321000, Zhejiang, China.
Miaomiao JinDepartment of Thyroid Breast Surgery, Jinhua Municipal Central Hospital, No. 365 East Renmin Road, Jinhua, 321000, Zhejiang, China.
Shuguang LiDepartment of Thyroid Breast Surgery, Jinhua Municipal Central Hospital, No. 365 East Renmin Road, Jinhua, 321000, Zhejiang, China.
Fan WangDepartment of Thyroid Breast Surgery, Jinhua Municipal Central Hospital, No. 365 East Renmin Road, Jinhua, 321000, Zhejiang, China. wangfan0997@163.com.ORCID http://orcid.org/0000-0003-4643-0500
Jinhua Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTo understand the effect of DNMT1-mediated MEG3 promoter methylation on breast cancer progression.

methodsExpression of DNMT1, MEG3 and miR-494-3p was assayed by qRT-PCR and western blot. Methylation-specific PCR was used to examine MEG3 promoter methylation level. ChIP, RNA binding protein immunoprecipitation assay and dual-luciferase reporter gene assay were applied to verify interaction between DNMT1 and MEG3, miR-494-3p and MEG3 and OTUD4. CCK-8, wound healing and Transwell assays were used to detect biological functions of breast cancer cells. Tumor growth was observed by tumor xenograft model.

resultsDNMT1 and miR-494-3p were highly expressed while MEG3 and OTUD4 were lowly expressed in breast cancer cells. Knockdown of DNMT1 inhibited progression of breast cancer cells by enhance MEG3 expression through demethylation. MEG3 could downregulate miR-494-3p expression, and OTUD4 was a target of miR-494-3p. Upregulation of MEG3 and downregulation of miR-494-3p both inhibited malignant behavior of cells in vitro. In addition, high MEG3 expression restrained growth of breast cancer in vivo.

conclusionBriefly, our results demonstrated that, DNMT1 induced methylation of MEG3 promoter, and played a key role in breast cancer growth throughmiR-494-3p/OTUD4 axis. These findings provide new insights into molecular therapeutic targets for breast cancer.

Indexed as

Breast cancerDNMT1GrowthMEG3Methylation

Identifiers

PMID35109842
PMCPMC8812010
OpenAlexW4210812124

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.