Evidence map›Paper›PMID 24391143›Full record

ArticleMolecular cancer research : MCR2014

Kinesin family deregulation coordinated by bromodomain protein ANCCA and histone methyltransferase MLL for breast cancer cell growth, survival, and tamoxifen resistance.

June X Zou, Zhijian Duan, Junjian Wang, Alex Sokolov, Jianzhen Xu, Christopher Z Chen, Jian Jian Li, Hong-Wu Chen

Open access · greenAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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

112 citing papers in PubMed, 1 synthesis or guideline pooled it, 214 citations in OpenAlex.

  1. Pooled it
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  13. Unsupervised cell line embedding using pairwise drug response correlation.Computational and structural biotechnology journal · 2025
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52 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

8 authors at 2 institutions in 2 countries.

June X ZouUC Davis Cancer Center/Basic Sciences, University of California, Davis, UCDMC Research III, Room 1400B, 4645 2nd Avenue, Sacramento, CA 95817. hwzchen@ucdavis.edu.
Zhijian Duan
Junjian Wang
Alex Sokolov
Jianzhen Xu
Christopher Z Chen
Jian Jian Li
Hong-Wu Chen
UC Davis Comprehensive Cancer CenterHenan University of Technology · CN

Funding

Protein acetylation as Mechanism of Hormone SignalingR01DK060019 · NIDDK · UNIVERSITY OF CALIFORNIA DAVIS · PI CHEN, HONGWU · 2002 to 2012
$2.8M
NF-kB-mediated HER-2 overexpression in radioresistant breast cancer stem cells?R01CA133402 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI LI, JIAN JIAN · 2009 to 2013
$1.5M
NCI NIH HHS R01 CA133402NCI NIH HHS R01CA133402NIDDK NIH HHS R01 DK060019NIDDK NIH HHS R01DK060019
6 · The paper itself

Abstract

unlabelledKinesins are a superfamily of motor proteins and often deregulated in different cancers. However, the mechanism of their deregulation has been poorly understood. Through examining kinesin gene family expression in estrogen receptor (ER)-positive breast cancer cells, we found that estrogen stimulation of cancer cell proliferation involves a concerted regulation of specific kinesins. Estrogen strongly induces expression of 19 kinesin genes such as Kif4A/4B, Kif5A/5B, Kif10, Kif11, Kif15, Kif18A/18B, Kif20A/20B, Kif21, Kif23, Kif24, Kif25, and KifC1, whereas suppresses the expression of seven others, including Kif1A, Kif1C, Kif7, and KifC3. Interestingly, the bromodomain protein ANCCA/ATAD2, previously shown to be an estrogen-induced chromatin regulator, plays a crucial role in the up- and downregulation of kinesins by estrogen. Its overexpression drives estrogen-independent upregulation of specific kinesins. Mechanistically, ANCCA (AAA nuclear coregulator cancer associated) mediates E2-dependent recruitment of E2F and MLL1 histone methyltransferase at kinesin gene promoters for gene activation-associated H3K4me3 methylation. Importantly, elevated levels of Kif4A, Kif15, Kif20A, and Kif23 correlate with that of ANCCA in the tumors and with poor relapse-free survival of patients with ER-positive breast cancer. Their knockdown strongly impeded proliferation and induced apoptosis of both tamoxifen-sensitive and resistant cancer cells. Together, the study reveals ANCCA as a key mediator of kinesin family deregulation in breast cancer and the crucial role of multiple kinesins in growth and survival of the tumor cells. IMPLICATIONS: These findings support the development of novel inhibitors of cancer-associated kinesins and their regulator ANCCA for effective treatment of cancers including tamoxifen-resistant breast cancers.

Indexed as

Adenosine TriphosphatasesATPases Associated with Diverse Cellular ActivitiesBreast NeoplasmsCell Growth ProcessesCell Line, TumorDNA-Binding ProteinsDown-RegulationDrug Resistance, NeoplasmEstradiolEstrogen AntagonistsFemaleHistone-Lysine N-MethyltransferaseHistone MethyltransferasesHumansKinesinsMCF-7 CellsAdenosine TriphosphatasesATAD2 protein, humanATPases Associated with Diverse Cellular ActivitiesDNA-Binding ProteinsEstradiolEstrogen AntagonistsHistone-Lysine N-MethyltransferaseHistone MethyltransferasesKinesinsTamoxifen

Identifiers

PMID24391143
PMCPMC4139106
OpenAlexW2130779727

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.