Evidence map›Paper›PMID 24413182›Full record

ArticleMolecular cancer research : MCR2014

KIF3a promotes proliferation and invasion via Wnt signaling in advanced prostate cancer.

Zun Liu, Ryan E Rebowe, Zemin Wang, Yingchun Li, Zehua Wang, John S DePaolo, Jianhui Guo, Chiping Qian, Wanguo Liu

Abstract 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 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

34 citing papers in PubMed, 63 citations in OpenAlex.

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  19. [Expression of kinesin KIF3A in the kidney of mice with unilateral ureteral obstruction].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020
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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

9 authors at 2 institutions in 1 country.

Zun LiuDepartment of Genetics and Stanley S. Scott Cancer Center, Louisiana State University Health Sciences Center, LCRC building Room 904, 1700 Tulane Avenue, New Orleans, LA 70112. wliu2@lsuhsc.edu.
Ryan E Rebowe
Zemin Wang
Yingchun Li
Zehua Wang
John S DePaolo
Jianhui Guo
Chiping Qian
Wanguo Liu
Louisiana State University Health Sciences Center New Orleans · USLouisiana State University · US

Funding

Training CoreP20MD004817 · NIMHD · DILLARD UNIVERSITY · PI JONES, WARREN ALLEN · 2010 to 2014
$6.3M
DNA Damage-Response Defects in Prostate Cancer RiskR01CA115555 · NCI · LSU HEALTH SCIENCES CENTER · PI LIU, WANGUO · 2007 to 2010
$1.5M
NCI NIH HHS R01 CA115555NCI NIH HHS R01 CA115555-03S1NIMHD NIH HHS P20 MD004817
6 · The paper itself

Abstract

unlabelledAberrant activation of the Wnt/β-catenin signaling pathway is a critical event in advanced prostate cancer, but the genetic alterations that activate the Wnt signaling pathway in many other cancers are rarely observed in prostate cancer. Other molecular mechanisms that regulate the Wnt signaling pathway in prostate cancer remain to be identified. Here, it is demonstrated that KIF3a, a subunit of kinesin-II motor protein, functions as an agonist of the Wnt signaling pathway in prostate cancer. KIF3a is upregulated in the majority of human prostate cancer cell lines and primary tumor biopsies. The expression levels of KIF3a correlate with a higher Gleason score, tumor-node-metastasis stage, and metastatic status of prostate cancer. Moreover, exogenous expression of KIF3a promoted cell growth in the benign prostate cells, whereas silencing KIF3a in cancer cells decreased cell proliferation, anchorage-independent cell growth, and cell migration/invasion. Mechanistically, KIF3a increases CK1-dependent DVL2 phosphorylation and β-catenin activation in prostate cancer cells, leading to transactivation of the Wnt-signaling target genes such as cyclin D1, HEF1, and MMP9. These findings support the notion that upregulation of KIF3a is causal of aberrant activation of Wnt signaling in advanced prostate cancer through the KIF3a-DVL2-β-catenin axis. IMPLICATIONS: Inactivation of KIF3a may improve survival of patients with advanced prostate cancer in which Wnt signaling is activated.

Indexed as

Wnt Signaling PathwayAdaptor Proteins, Signal Transducingbeta CateninCell Growth ProcessesCell Line, TumorCyclin D1Disease ProgressionDishevelled ProteinsHEK293 CellsHumansKinesinsMaleMatrix Metalloproteinase 9Neoplasm InvasivenessPhosphoproteinsPhosphorylationAdaptor Proteins, Signal Transducingbeta CateninCCND1 protein, humanCTNNB1 protein, humanCyclin D1Dishevelled ProteinsDVL2 protein, humanKIF3A protein, humanKinesinsMatrix Metalloproteinase 9MMP9 protein, humanNEDD9 protein, humanPhosphoproteinsWnt Proteins

Identifiers

PMID24413182
PMCPMC4001865
OpenAlexW2134873805

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.