Evidence map›Paper›PMID 26461058›Full record

ArticleBritish journal of cancer2015

Pin1 facilitates NF-κB activation and promotes tumour progression in human hepatocellular carcinoma.

Kimio Shinoda, Satoshi Kuboki, Hiroaki Shimizu, Masayuki Ohtsuka, Atsushi Kato, Hideyuki Yoshitomi, Katsunori Furukawa, Masaru Miyazaki

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Prognostic value of peptidyl-prolyl cis-trans isomerase 1 (PIN1) in human malignant tumors.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020
    Pooled it
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  7. Valence-Change MnOJournal of the American Chemical Society · 2024
    Article
  8. Post-translational modifications of p65: state of the art.Frontiers in cell and developmental biology · 2024
    Review
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  10. Review
  11. Review
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  14. Pinning Down the Transcription: A Role for Peptidyl-ProlylFrontiers in cell and developmental biology · 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

8 authors at 1 institution in 1 country.

Kimio ShinodaDepartment of General Surgery, Graduate School of Medicine, Chiba University, Chiba 260-0856, Japan.
Satoshi KubokiDepartment of General Surgery, Graduate School of Medicine, Chiba University, Chiba 260-0856, Japan.
Hiroaki ShimizuDepartment of General Surgery, Graduate School of Medicine, Chiba University, Chiba 260-0856, Japan.
Masayuki OhtsukaDepartment of General Surgery, Graduate School of Medicine, Chiba University, Chiba 260-0856, Japan.
Atsushi KatoDepartment of General Surgery, Graduate School of Medicine, Chiba University, Chiba 260-0856, Japan.
Hideyuki YoshitomiDepartment of General Surgery, Graduate School of Medicine, Chiba University, Chiba 260-0856, Japan.
Katsunori FurukawaDepartment of General Surgery, Graduate School of Medicine, Chiba University, Chiba 260-0856, Japan.
Masaru MiyazakiDepartment of General Surgery, Graduate School of Medicine, Chiba University, Chiba 260-0856, Japan.
Chiba University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNF-κB promotes HCC progression; however, therapies targeting NF-κB are not used due to severe adverse reactions. Pin1 is reported to induce tumour progression in vitro. However, the role of Pin1 in HCC is unclear. Moreover, little is known about the mechanism of Pin1-mediated NF-κB activation.

methodsFresh surgical specimens were collected from 144 HCC patients. Pin1 and NF-κB-p65 expression was evaluated by immunohistochemistry and western blotting. NF-κB activation was assessed by EMSA.

resultsPin1 was increased in HCC compared to adjacent liver tissue. The multivariate analysis revealed that high Pin1 expression was an independent factor for poor prognosis. In HCC with high Pin1 expression, tumour size was larger and portal vein invasion was increased. Pin1 expression was correlated with phosphorylated (p-) NF-κB-p65(Thr254) and p-NF-κB-p65(Ser276), and thereby NF-κB activation. Pin1-induced NF-κB activation accelerated cell cycle progression, induced angiogenesis, and inhibited apoptosis. Pin1 knockdown in HCC cells inhibited the phosphorylation of NF-κB-p65(Ser276), and reduced NF-κB activation, which resulted in inhibiting tumour cell progression. When HCC cells were treated with the Pin1 inhibitors, p-NF-κB-p65(Ser276) expression and NF-κB activation was reduced, and cell proliferation was inhibited.

conclusionsPin1 is associated with aggressive tumour progression and poor prognosis in HCC by mediating NF-κB activation.

Indexed as

AgedApoptosisCarcinoma, HepatocellularCell CycleCell Line, TumorDisease ProgressionFemaleHep G2 CellsHumansLiver NeoplasmsMaleNeovascularization, PathologicNF-kappa BNIMA-Interacting Peptidylprolyl IsomerasePeptidylprolyl IsomerasePhosphorylationNF-kappa BNIMA-Interacting Peptidylprolyl IsomerasePeptidylprolyl IsomerasePIN1 protein, humanTranscription Factor RelA

Identifiers

PMID26461058
PMCPMC4815797
OpenAlexW2419248317

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.