Evidence map›Paper›PMID 35115926›Full record

ArticleFrontiers in pharmacology2021

PBK Enhances Cellular Proliferation With Histone H3 Phosphorylation and Suppresses Migration and Invasion With CDH1 Stabilization in Colorectal Cancer.

Akira Koshino, Aya Nagano, Akinobu Ota, Toshinori Hyodo, Akane Ueki, Masayuki Komura, Akane Sugimura-Nagata, Masahide Ebi, Naotaka Ogasawara, Kenji Kasai and 4 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

11 citing papers in PubMed, 27 citations in OpenAlex.

  1. The Correlation ofCancers · 2026
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  2. Review
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  10. SPATA18 Expression Predicts Favorable Clinical Outcome in Colorectal Cancer.International journal of molecular sciences · 2022
    Article
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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

14 authors at 2 institutions in 1 country.

Akira KoshinoDivision of Gastroenterology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Japan.
Aya NaganoDepartment of Experimental Pathology and Tumor Biology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Akinobu OtaDepartment of Biochemistry, Aichi Medical University School of Medicine, Nagakute, Japan.
Toshinori HyodoDepartment of Biochemistry, Aichi Medical University School of Medicine, Nagakute, Japan.
Akane UekiDepartment of Experimental Pathology and Tumor Biology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Masayuki KomuraDepartment of Experimental Pathology and Tumor Biology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Akane Sugimura-NagataDivision of Gastroenterology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Japan.
Masahide EbiDivision of Gastroenterology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Japan.
Naotaka OgasawaraDivision of Gastroenterology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Japan.
Kenji KasaiDepartment of Pathology, Aichi Medical University School of Medicine, Nagakute, Japan.
Yoshitaka HosokawaDepartment of Biochemistry, Aichi Medical University School of Medicine, Nagakute, Japan.
Kunio KasugaiDivision of Gastroenterology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Japan.
Satoru TakahashiDepartment of Experimental Pathology and Tumor Biology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Shingo InagumaDepartment of Experimental Pathology and Tumor Biology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Aichi Medical University · JPNagoya City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is one of the most frequent gastrointestinal malignancies with high morbidity and mortality rates. Several biological markers for the prognostication of patient outcome of CRCs are available. Recently, our group identified two favorable factors for the survival of CRC patients: PDZ-binding kinase (PBK) and phospho-histone H3 (PHH3). Both showed a significant inverse association to pT stage. The aim of this study was to uncover the mechanism through which these cellular proliferation-associated protein expressions lead to favorable clinical outcome in CRC patients. We first confirmed co-expression of PBK and PHH3 in CRC cells. Further investigation showed that aberrantly expressed PBK up-regulated the cellular proliferation of CRC cells with accumulation of PHH3. The PBK inhibitor OTS514 suppressed cellular proliferation of CRC cells through down-regulation of PHH3 and induction of apoptosis.

Indexed as

cellular proliferationcolorectal cancerE-cadherininvasionmigrationPDZ-binding kinasephospho-histone H3

Identifiers

PMID35115926
PMCPMC8804381
OpenAlexW4206357199

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.