Evidence map›Paper›PMID 25645929›Full record

ArticleMolecular and cellular biology2015

The hippo pathway effector YAP regulates motility, invasion, and castration-resistant growth of prostate cancer cells.

Lin Zhang, Shuping Yang, Xingcheng Chen, Seth Stauffer, Fang Yu, Subodh M Lele, Kai Fu, Kaustubh Datta, Nicholas Palermo, Yuanhong Chen and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
8.3field-weighted citation impact, top 2% 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

106 citing papers in PubMed, 166 citations in OpenAlex.

  1. DNA Methylation-Based Risk Stratification and Classification of Pediatric Thyroid Carcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article
  2. Article
  3. The Regulation and Function of Hippo/YAP Pathway in Cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
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46 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

11 authors at 2 institutions in 2 countries.

Lin ZhangEppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, Nebraska, USA Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Shuping YangEppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, Nebraska, USA Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska, USA Department of Oncology, Shandong Provincial Hospital affiliated with Shandong University, Jinan, Shandong, People's Republic of China.
Xingcheng ChenEppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, Nebraska, USA Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Seth StaufferEppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, Nebraska, USA Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Fang YuDepartment of Biostatistics, School of Public Health, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Subodh M LeleDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Kai FuDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Kaustubh DattaDepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Nicholas PalermoHolland Computing Center, University of Nebraska-Lincoln, Lincoln, Nebraska, USA.
Yuanhong ChenEppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Jixin DongEppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, Nebraska, USA dongj@unmc.edu.
University of Nebraska Medical Center · USUniversity of Nebraska–Lincoln · US

Funding

Research Pilot Project ProgramP30GM106397 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI JOHNSON, KEITH R · 2013 to 2017
$4.9M
Regulation and Functional Dissection of YAP in MitosisR01GM109066 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI DONG, JIXIN · 2014 to 2018
$1.4M
NIGMS NIH HHS P30 GM106397NIGMS NIH HHS R01 GM109066
6 · The paper itself

Abstract

Yes-associated protein (YAP) is an effector of the Hippo tumor suppressor pathway. The functional significance of YAP in prostate cancer has remained elusive. In this study, we first show that enhanced expression of YAP is able to transform immortalized prostate epithelial cells and promote migration and invasion in both immortalized and cancerous prostate cells. We found that YAP mRNA was upregulated in androgen-insensitive prostate cancer cells (LNCaP-C81 and LNCaP-C4-2 cells) compared to the level in androgen-sensitive LNCaP cells. Importantly, ectopic expression of YAP activated androgen receptor signaling and was sufficient to promote LNCaP cells from an androgen-sensitive state to an androgen-insensitive state in vitro, and YAP conferred castration resistance in vivo. Accordingly, YAP knockdown greatly reduced the rates of migration and invasion of LNCaP-C4-2 cells and under androgen deprivation conditions largely blocked cell division in LNCaP-C4-2 cells. Mechanistically, we found that extracellular signal-regulated kinase-ribosomal s6 kinase signaling was downstream of YAP for cell survival, migration, and invasion in androgen-insensitive cells. Finally, immunohistochemistry showed significant upregulation and hyperactivation of YAP in castration-resistant prostate tumors compared to their levels in hormone-responsive prostate tumors. Together, our results identify YAP to be a novel regulator in prostate cancer cell motility, invasion, and castration-resistant growth and as a potential therapeutic target for metastatic castration-resistant prostate cancer (CRPC).

Indexed as

Gene Expression Regulation, NeoplasticSignal TransductionAdaptor Proteins, Signal TransducingAndrogensAnimalsCastrationCell MovementCell ProliferationGene Knockdown TechniquesHEK293 CellsHippo Signaling PathwayHumansMaleMAP Kinase Signaling SystemMice, SCIDNeoplasm InvasivenessAdaptor Proteins, Signal TransducingAndrogensPhosphoproteinsProtein Serine-Threonine KinasesTranscription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID25645929
PMCPMC4372700
OpenAlexW2112413714

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.