Evidence map›Paper›PMID 19840198›Full record

ArticleJournal of cellular and molecular medicine2010

Androgen receptor coactivator p44/Mep50 in breast cancer growth and invasion.

Yi Peng, Yirong Li, Lan Lin Gellert, Xuanyi Zou, Jun Wang, Baljit Singh, Ruliang Xu, Luis Chiriboga, Garrett Daniels, Ruimin Pan and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. The Role of WDR77 in Cancer: More than a PRMT5 Interactor.Molecular cancer research : MCR · 2025
    Review
  3. TBL2 Promotes Tumorigenesis via PRMT5/WDR77-Mediated AKT Activation in Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  4. Article
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  6. Article
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  9. Review
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  12. Yeast two-hybrid screening identified WDR77 as a novel interacting partner of TSC22D2.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Protein-intrinsic and signaling network-based sources of resistance to EGFR- and ErbB family-targeted therapies in head and neck cancer.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2011
    Review
  18. Article
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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

15 authors at 4 institutions in 1 country.

Yi PengDepartment of Pathology, New York University School of Medicine, New York, NY 10010, USA.
Yirong Li
Lan Lin Gellert
Xuanyi Zou
Jun Wang
Baljit Singh
Ruliang Xu
Luis Chiriboga
Garrett Daniels
Ruimin Pan
David Y Zhang
Michael J Garabedian
Robert J Schneider
Zhengxin Wang
Peng Lee
New York University · USIcahn School of Medicine at Mount Sinai · USThe University of Texas MD Anderson Cancer Center · USVA NY Harbor Healthcare System · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hormones and their receptors play an important role in the development and progression of breast carcinoma. Although the primary focus has been on oestrogen and oestrogen receptor (ER), androgen, androgen receptor (AR) and its coactivator(s) have been implicated in tumorigenesis of breast carcinoma and warrant further investigation. AR coactivator p44/Mep50 is identified as a subunit of methylosome complex and lately characterized as an AR coactivator that enhances AR mediated transcription activity in a ligand dependent manner. In prostate cancer, p44 is expressed in the nucleus of benign epithelia and translocated into the cytoplasm in cancer cells. Furthermore, nuclear expression of p44 inhibits prostate cancer growth. In this report, we examined the expression and function of p44 in breast cancer. In addition to being an AR coactivator, p44 also functions as an ER coactivator. In contrast to findings in prostate cancer, the expression of p44 shows strong cytoplasmic expression in morphologically normal terminal ductal lobular units, while nuclear p44 is observed in both ductal carcinoma in situ and invasive carcinoma. Further, overexpression of nuclear-localized p44 stimulates proliferation and invasion in MCF7 breast cancer cells in the presence of oestrogen and the process is ERα dependent. These findings strongly suggest that p44 plays a role in mediating the effects of hormones during tumorigenesis in breast.

Indexed as

Breast NeoplasmsCarcinoma, Ductal, BreastCell Line, TumorCell ProliferationEstrogensFemaleGene ExpressionGene Expression Regulation, NeoplasticHumansMammary Glands, HumanNeoplasm InvasivenessReceptors, EstrogenReverse Transcriptase Polymerase Chain ReactionSignal TransductionTranscription FactorsEstrogensReceptors, EstrogenTranscription FactorsWDR77 protein, human

Identifiers

PMID19840198
PMCPMC3822728
OpenAlexW2031145093

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.