Evidence map›Paper›PMID 24854087›Full record

ArticleExperimental & molecular medicine2014

Silencing of KIF14 interferes with cell cycle progression and cytokinesis by blocking the p27(Kip1) ubiquitination pathway in hepatocellular carcinoma.

Haidong Xu, Chungyoul Choe, Seung-Hun Shin, Sung-Won Park, Ho-Shik Kim, Seung-Hyun Jung, Seon-Hee Yim, Tae-Min Kim, Yeun-Jun Chung

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

40 citing papers in PubMed, 63 citations in OpenAlex.

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  11. The role of kinesin superfamily proteins in hepatocellular carcinoma.Medical oncology (Northwood, London, England) · 2024
    Review
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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 1 institution in 1 country.

Haidong Xu1] Integrated Research Center for Genome Polymorphism, Department of Microbiology, Catholic University of Korea, College of Medicine, Seoul, Korea [2] Center of Laboratory, Yanbian University Hospital, Yanji, China.
Chungyoul ChoeIntegrated Research Center for Genome Polymorphism, Department of Microbiology, Catholic University of Korea, College of Medicine, Seoul, Korea.
Seung-Hun ShinIntegrated Research Center for Genome Polymorphism, Department of Microbiology, Catholic University of Korea, College of Medicine, Seoul, Korea.
Sung-Won ParkIntegrated Research Center for Genome Polymorphism, Department of Microbiology, Catholic University of Korea, College of Medicine, Seoul, Korea.
Ho-Shik KimDepartment of Biochemistry, Catholic University of Korea, College of Medicine, Seoul, Korea.
Seung-Hyun JungIntegrated Research Center for Genome Polymorphism, Department of Microbiology, Catholic University of Korea, College of Medicine, Seoul, Korea.
Seon-Hee Yim1] Integrated Research Center for Genome Polymorphism, Department of Microbiology, Catholic University of Korea, College of Medicine, Seoul, Korea [2] Department of Medical Education, Catholic University of Korea, College of Medicine, Seoul, Korea.
Tae-Min KimMRC Cancer Evolution Research Center, Department of Medical Informatics, Catholic University of Korea, College of Medicine, Seoul, Korea.
Yeun-Jun ChungIntegrated Research Center for Genome Polymorphism, Department of Microbiology, Catholic University of Korea, College of Medicine, Seoul, Korea.
Catholic University of Korea · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although it has been suggested that kinesin family member 14 (KIF14) has oncogenic potential in various cancers, including hepatocellular carcinoma (HCC), the molecular mechanism of this potential remains unknown. We aimed to elucidate the role of KIF14 in hepatocarcinogenesis by knocking down KIF14 in HCC cells that overexpressed KIF14. After KIF14 knockdown, changes in tumor cell growth, cell cycle and cytokinesis were examined. We also examined cell cycle regulatory molecules and upstream Skp1/Cul1/F-box (SCF) complex molecules. Knockdown of KIF14 resulted in suppression of cell proliferation and failure of cytokinesis, whereas KIF14 overexpression increased cell proliferation. In KIF14-silenced cells, the levels of cyclins E1, D1 and B1 were profoundly decreased compared with control cells. Of the cyclin-dependent kinase inhibitors, the p27(Kip1) protein level specifically increased after KIF14 knockdown. The increase in p27(Kip1) was not due to elevation of its mRNA level, but was due to inhibition of the proteasome-dependent degradation pathway. To explore the pathway upstream of this event, we measured the levels of SCF complex molecules, including Skp1, Skp2, Cul1, Roc1 and Cks1. The levels of Skp2 and its cofactor Cks1 decreased in the KIF14 knockdown cells where p27(Kip1) accumulated. Overexpression of Skp2 in the KIF14 knockdown cells attenuated the failure of cytokinesis. On the basis of these results, we postulate that KIF14 knockdown downregulates the expression of Skp2 and Cks1, which target p27(Kip1) for degradation by the 26S proteasome, leading to accumulation of p27(Kip1). The downregulation of Skp2 and Cks1 also resulted in cytokinesis failure, which may inhibit tumor growth. To the best of our knowledge, this is the first report that has identified the molecular target and oncogenic effect of KIF14 in HCC.

Indexed as

CytokinesisUbiquitinationCarcinoma, HepatocellularCyclin-Dependent Kinase Inhibitor p27CyclinsGene SilencingHep G2 CellsHumansKinesinsLiver NeoplasmsOncogene ProteinsProteasome Endopeptidase ComplexRNA, MessengerS-Phase Kinase-Associated ProteinsCyclin-Dependent Kinase Inhibitor p27CyclinsKIF14 protein, humanKinesinsOncogene ProteinsProteasome Endopeptidase ComplexRNA, MessengerS-Phase Kinase-Associated Proteins

Identifiers

PMID24854087
PMCPMC4044675
OpenAlexW1982679787

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.