Evidence map›Paper›PMID 20423983›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2010

Aurora kinase A promotes ovarian tumorigenesis through dysregulation of the cell cycle and suppression of BRCA2.

Gong Yang, Bin Chang, Fan Yang, Xiaoqing Guo, Kathy Qi Cai, Xue Sherry Xiao, Huamin Wang, Subrata Sen, Mien-Chie Hung, Gordon B Mills and 4 more

Abstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

76 citing papers in PubMed, 123 citations in OpenAlex.

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16 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

14 authors at 4 institutions in 2 countries.

Gong YangDepartment of Pathology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Bin Chang
Fan Yang
Xiaoqing Guo
Kathy Qi Cai
Xue Sherry Xiao
Huamin Wang
Subrata Sen
Mien-Chie Hung
Gordon B Mills
Sandy Chang
Asha S Multani
Imelda Mercado-Uribe
Jinsong Liu
China Medical University · TWFox Chase Cancer Center · USThe University of Texas MD Anderson Cancer Center · USChina Medical University Hospital · TW

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Therapeutic Micro RNA Strategies for Ovarian CancerP50CA083638 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI GODWIN, ANDREW K., GOLEMIS, ERICA A. · 1999 to 2013
$33.6M
Targeting the PI3K Signaling Pathway in Endometrial CarcinomaP50CA098258 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BODURKA, DIANE · 2003 to 2020
$32.0M
UTMDACC SPORE in Breast CancerP50CA116199 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BERRY, DONALD A · 2005 to 2009
$11.9M
RAS Signaling, Senescent Fibroblasts, and Ovarian Cancer ProgressionR01CA131183 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LIU, JINSONG · 2008 to 2012
$1.3M
NCI NIH HHS 5P50CA116199-05NCI NIH HHS CA016672NCI NIH HHS IP50CA83638NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA083638NCI NIH HHS P50 CA098258NCI NIH HHS P50 CA116199NCI NIH HHS R01 CA131183NCI NIH HHS R01CA131183-01A2
6 · The paper itself

Abstract

purposeAurora kinase A (Aurora-A) is known to regulate genomic instability and tumorigenesis in multiple human cancers. The underlying mechanism, however, is not fully understood. We examined the molecular mechanism of Aurora-A regulation in human ovarian cancer. EXPERIMENTAL

designRetrovirus-mediated small hairpin RNA (shRNA) was used to silence the expression of Aurora-A in the ovarian cancer cell lines SKOV3, OVCA432, and OVCA433. Immunofluorescence, Western blotting, flow cytometry, cytogenetic analysis, and animal assay were used to test centrosome amplification, cell cycle alteration, apoptosis, DNA damage response, tumor growth, and genomic instability. Immunostaining of BRCA2 and Aurora-A was done in ovarian, pancreatic, breast, and colon cancer samples.

resultsKnockdown of Aurora-A reduced centrosome amplification, malformation of mitotic spindles, and chromosome aberration, leading to decreased tumor growth. Silencing Aurora-A attenuated cell cycle progression and enhanced apoptosis and DNA damage response by restoring p21, pRb, and BRCA2 expression. Aurora-A was inversely correlated with BRCA2 in high-grade ovarian serous carcinoma, breast cancer, and pancreatic cancer. In high-grade ovarian serous carcinoma, positive expression of BRCA2 predicted increased overall and disease-free survival, whereas positive expression of Aurora-A predicted poor overall and disease-free survival (P < 0.05). Moreover, an increased Aurora-A to BRCA2 expression ratio predicted poor overall survival (P = 0.047) compared with a decreased Aurora-A to BRCA2 expression ratio.

conclusionAurora-A regulates genomic instability and tumorigenesis through cell cycle dysregulation and BRCA2 suppression. The negative correlation between Aurora-A and BRCA2 exists in multiple cancers, whereas the expression ratio of Aurora-A to BRCA2 predicts ovarian cancer patient outcome.

Indexed as

Cell CycleApoptosisAurora Kinase AAurora KinasesBRCA2 ProteinCell Line, TumorCell ProliferationCell Transformation, NeoplasticDNA DamageFemaleGene SilencingGenomic InstabilityHumansOvarian NeoplasmsProtein Serine-Threonine KinasesAURKA protein, humanAurora Kinase AAurora KinasesBRCA2 ProteinProtein Serine-Threonine Kinases

Identifiers

PMID20423983
PMCPMC2930838
OpenAlexW2135179721

What OpenQuestion holds

Textmetadata
LicenceTDM
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.