Evidence map›Paper›PMID 22440256›Full record

ArticleThe American journal of pathology2012

Yin Yang 1 plays an essential role in breast cancer and negatively regulates p27.

Meimei Wan, Weiwei Huang, Timothy E Kute, Lance D Miller, Qiang Zhang, Heather Hatcher, Jingxuan Wang, Daniel B Stovall, Gregory B Russell, Paul D Cao and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

63 citing papers in PubMed, 100 citations in OpenAlex.

  1. Article
  2. Bioinformatics and biology insights · 2026
    Article
  3. The YYR (YY1- RKIP) Regulatory Axis in the pathogenesis of Cancer and Immune Evasion.Journal of experimental & clinical cancer research : CR · 2025
    Review
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3 more citing papers are in PubMed but not listed here.

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

17 authors at 4 institutions in 3 countries.

Meimei WanComprehensive Cancer Center Department of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA.
Weiwei Huang
Timothy E Kute
Lance D Miller
Qiang Zhang
Heather Hatcher
Jingxuan Wang
Daniel B Stovall
Gregory B Russell
Paul D Cao
Zhiyong Deng
Wei Wang
Qingyuan Zhang
Ming Lei
Suzy V Torti
Steven A Akman
Guangchao Sui
Wake Forest University · USAgriculture and Forestry University · NPThird Affiliated Hospital of Harbin Medical University · CNHarbin Medical University · CN

Funding

Tumor Tissue CoreP30CA012197 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Ruben A. Mesa · 1985 to 2026
$55.4M
NCI NIH HHS P30 CA012197
6 · The paper itself

Abstract

Yin Yang 1 (YY1) is highly expressed in various types of cancers and regulates tumorigenesis through multiple pathways. In the present study, we evaluated YY1 expression levels in breast cancer cell lines, a breast cancer TMA, and two gene arrays. We observed that, compared with normal samples, YY1 is generally overexpressed in breast cancer cells and tissues. In functional studies, depletion of YY1 inhibited the clonogenicity, migration, invasion, and tumor formation of breast cancer cells, but did not affect the clonogenicity of nontumorigenic cells. Conversely, ectopically expressed YY1 enhanced the migration and invasion of nontumorigenic MCF-10A breast cells. In both a monolayer culture condition and a three-dimensional Matrigel system, silenced YY1 expression changed the architecture of breast cancer MCF-7 cells to that resembling MCF-10A cells, whereas ectopically expressed YY1 in MCF-10A cells had the opposite effect. Furthermore, we detected an inverse correlation between YY1 and p27 expression in both breast cancer cells and xenograft tumors with manipulated YY1 expression. Counteracting the changes in p27 expression attenuated the effects of YY1 alterations on these cells. In addition, YY1 promoted p27 ubiquitination and physically interacted with p27. In conclusion, our data suggest that YY1 is an oncogene and identify p27 as a new target of YY1.

Indexed as

AnimalsBreast NeoplasmsCell CycleCell MovementCell ProliferationCell ShapeCell Transformation, NeoplasticFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMiceMice, NudeNeoplasm InvasivenessNeoplasm ProteinsNeoplasm TransplantationNeoplasm Proteinsp27 antigenProliferating Cell Nuclear AntigenYY1 protein, humanYY1 Transcription Factor

Identifiers

PMID22440256
PMCPMC3828504
OpenAlexW2035315325

What OpenQuestion holds

Textmetadata
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.