Evidence map›Paper›PMID 33608512›Full record

ArticleCell death & disease2021

Distinct Ring1b complexes defined by DEAD-box helicases and EMT transcription factors synergistically enhance E-cadherin silencing in breast cancer.

Yawei Wang, Yingying Sun, Chao Shang, Lili Chen, Hongyu Chen, Dake Wang, Xianlu Zeng

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

10 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Critical Roles of Polycomb Repressive Complexes in Transcription and Cancer.International journal of molecular sciences · 2022
    Review
  9. Cancers · 2022
    Article
  10. Review
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

7 authors at 1 institution in 1 country.

Yawei WangThe Key Laboratory of Molecular Epigenetics of the Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun, Jilin, China.
Yingying SunThe Key Laboratory of Molecular Epigenetics of the Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun, Jilin, China.
Chao ShangThe Key Laboratory of Molecular Epigenetics of the Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun, Jilin, China.
Lili ChenThe Key Laboratory of Molecular Epigenetics of the Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun, Jilin, China.
Hongyu ChenThe Key Laboratory of Molecular Epigenetics of the Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun, Jilin, China.
Dake WangThe Key Laboratory of Molecular Epigenetics of the Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun, Jilin, China.
Xianlu ZengThe Key Laboratory of Molecular Epigenetics of the Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun, Jilin, China. zengx779@nenu.edu.cn.ORCID http://orcid.org/0000-0002-2655-4197
Northeast Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ring1b is a core subunit of polycomb repressive complex 1 (PRC1) and is essential in several high-risk cancers. However, the epigenetic mechanism of Ring1b underlying breast cancer malignancy is poorly understood. In this study, we showed increased expression of Ring1b promoted metastasis by weakening cell-cell adhesions of breast cancer cells. We confirmed that Ring1b could downregulate E-cadherin and contributed to an epigenetic rewiring via PRC1-dependent function by forming distinct complexes with DEAD-box RNA helicases (DDXs) or epithelial-mesenchymal transition transcription factors (EMT TFs) on site-specific loci of E-cadherin promoter. DDXs-Ring1b complexes moderately inhibited E-cadherin, which resulted in an early hybrid EMT state of epithelial cells, and EMT TFs-Ring1b complexes cooperated with DDXs-Ring1b complexes to further repress E-cadherin in mesenchymal-like cancer cells. Clinically, high expression of Ring1b with DDXs or EMT TFs predicted low levels of E-cadherin, metastatic behavior, and poor prognosis. These findings provide an epigenetic regulation mechanism of Ring1b complexes in E-cadherin expression. Ring1b complexes may be potential therapeutic targets and biomarkers for diagnosis and prognosis in invasion breast cancer.

Indexed as

Epithelial-Mesenchymal TransitionGene SilencingAnimalsAntigens, CDBinding SitesBreast NeoplasmsCadherinsCell MovementDEAD-box RNA HelicasesFemaleGene Expression Regulation, NeoplasticHEK293 CellsHumansMCF-7 CellsMiceMice, Inbred BALB CAntigens, CDCadherinsCDH1 protein, humanDDX3X protein, humanDdx5 protein, humanDEAD-box RNA HelicasesPolycomb Repressive Complex 1Repressor ProteinsRNF2 protein, humanSNAI1 protein, humanSnail Family Transcription FactorsTWIST2 protein, humanTwist-Related Protein 1

Identifiers

PMID33608512
PMCPMC7895950
OpenAlexW3131502825

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.