Evidence map›Paper›PMID 24667656›Full record

ArticlePloS one2014

STK31 is a cell-cycle regulated protein that contributes to the tumorigenicity of epithelial cancer cells.

Pao-Lin Kuo, Yung-Ling Huang, Christine Chin-Jung Hsieh, Jenq-Chang Lee, Bo-Wen Lin, Liang-Yi Hung

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  4. Analysis ofOncology letters · 2021
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  5. Oncology reports · 2021
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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

6 authors at 3 institutions in 1 country.

Pao-Lin KuoDepartment of Medical Laboratory Science BioTechnology, College of Medicine, National Cheng Kung University, Tainan, Taiwan; Department of Obstetrics and Gynecology, National Cheng-Kung University Hospital, Tainan, Taiwan.
Yung-Ling HuangDepartment of Medical Laboratory Science BioTechnology, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Christine Chin-Jung HsiehDepartment of Medical Laboratory Science BioTechnology, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Jenq-Chang LeeDepartment of Surgery, National Cheng-Kung University Hospital, Tainan, Taiwan.
Bo-Wen LinDepartment of Surgery, National Cheng-Kung University Hospital, Tainan, Taiwan.
Liang-Yi HungInstitute of Bioinformatics and Biosignal Transduction, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, Taiwan; Center for Infectious Disease and Signal Transduction Research, National Cheng Kung University, Tainan, Taiwan; Institute for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
National Cheng Kung University Hospital · TWNational Cheng Kung University · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Serine/threonine kinase 31 (STK31) is one of the novel cancer/testis antigens for which its biological functions remain largely unclear. Here, we demonstrate that STK31 is overexpressed in many human colorectal cancer cell lines and tissues. STK31 co-localizes with pericentrin in the centrosomal region throughout all phases of the cell cycle. Interestingly, when cells undergo mitosis, STK31 also localizes to the centromeres, central spindle, and midbody. This localization behavior is similar to that of chromosomal passenger proteins, which are known to be the important players of the spindle assembly checkpoint. The expression of STK31 is cell cycle-dependent through the regulation of a putative D-box near its C-terminal region. Ectopically-expressed STK31-GFP increases cell migration and invasive ability without altering the proliferation rate of cancer cells, whereas the knockdown expression of endogenous STK31 by lentivirus-derived shRNA results in microtubule assembly defects that prolong the duration of mitosis and lead to apoptosis. Taken together, our results suggest that the aberrant expression of STK31 contributes to tumorigenicity in somatic cancer cells. STK31 might therefore act as a potential therapeutic target in human somatic cancers.

Indexed as

CarcinogenesisCell CycleCell Line, TumorCell MovementCentrosomeColorectal NeoplasmsGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansKinetochoresMicrotubulesMitosisNeoplasm InvasivenessNeoplasms, Glandular and EpithelialProtein Serine-Threonine KinasesProtein TransportProtein Serine-Threonine KinasesRNA, Small InterferingSTK31 protein, human

Identifiers

PMID24667656
PMCPMC3965560
OpenAlexW2111656654

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.