Evidence map›Paper›PMID 35229028›Full record

ArticleMolecular therapy oncolytics2022

UXT, a novel DNMT3b-binding protein, promotes breast cancer progression via negatively modulating lncRNA MEG3/p53 axis.

Zhong-Feng Huang, Yu-Ling Tang, Zhao-Long Shen, Kai-Yan Yang, Kai Gao

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy oncolytics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

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  14. Roles and Mechanisms of Long Non-Coding RNAs in Breast Cancer.International journal of molecular sciences · 2022
    Review
  15. Review
  16. Review
  17. Comprehensive analysis of mFrontiers in immunology · 2022
    Article
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

5 authors at 3 institutions in 1 country.

Zhong-Feng HuangDepartment of Plastic Surgery, Xiangya Hospital of Central South University, Changsha 410008, Hunan Province, P. R. China.
Yu-Ling TangDepartment of Hepatobiliary and Pancreatic Surgery, The Third Xiangya Hospital of Central South University, Changsha 410013, Hunan Province, P. R. China.
Zhao-Long ShenDepartment of Gastrointestinal Surgery, The Third Xiangya Hospital of Central South University, No. 138, Tongzipo Road, Yuelu District, Changsha 410013, Hunan Province, P. R. China.
Kai-Yan YangDepartment of Gastrointestinal Surgery, The Third Xiangya Hospital of Central South University, No. 138, Tongzipo Road, Yuelu District, Changsha 410013, Hunan Province, P. R. China.
Kai GaoDepartment of Gastrointestinal Surgery, The Third Xiangya Hospital of Central South University, No. 138, Tongzipo Road, Yuelu District, Changsha 410013, Hunan Province, P. R. China.
Central South University · CNThird Xiangya Hospital · CNXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Overexpressed ubiquitously expressed transcript (UXT) in breast tumors and derived cell lines modulated the transcriptional activity of estrogen receptor alpha. However, how UXT exerts its biological functions in the tumorigenicity of breast cancer remains largely unknown. Expressions of UXT and maternally expressed gene 3 (MEG3) were examined by qRT-PCR and Western blot. The capacity of cell proliferation, apoptosis, migration, and invasion was assessed using CCK-8, flow cytometry, and transwell assays. Methylation-specific PCR (MS-PCR) was employed to evaluate the methylation of the MEG3 imprinting control region. Co-immunoprecipitation was performed to verify the UXT/DNMT3b interaction. RNA immunoprecipitation (RIP) was subjected to assess the regulation of MEG3 on p53 activity. A xenograft tumor model was further conducted to certify the molecular mechanism. UXT was upregulated, while MEG3 was downregulated in breast cancer tissues and cell lines. UXT knockdown or MEG3 overexpression inhibited cell proliferation, promoted apoptosis, and weakened cell migration and invasion. Hypermethylation of the MEG3 imprinting control region was modulated by highly expressed DNMT3b. UXT inhibited MEG3 expression via recruiting DNMT3b to its imprinting control region. MEG3 positively regulated p53 activity. UXT negatively regulated the MEG3/p53 axis in a DNMT3b-dependent manner to promote tumor growth. UXT, a novel DNMT3b-binding protein, aggravates the progression of breast cancer through MEG3/p53 axis.

Indexed as

breast cancerDNMT3blncRNA MEG3p53UXT

Identifiers

PMID35229028
PMCPMC8850569
OpenAlexW4200464024

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.