Evidence map›Paper›PMID 26576099›Full record

ReviewWorld journal of gastroenterology2015

Oncogenic role of p21 in hepatocarcinogenesis suggests a new treatment strategy.

Shogo Ohkoshi, Masahiko Yano, Yasunobu Matsuda

Open access · hybridAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-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

24 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. LOX-1 and Its Splicing Variant LOX-1International journal of hepatology · 2026
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  4. Review
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  11. AnFrontiers in genetics · 2021
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  20. Identification of Biological Targets of Therapeutic Intervention for Hepatocellular Carcinoma by Integrated Bioinformatical Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
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

3 authors at 1 institution in 1 country.

Shogo OhkoshiShogo Ohkoshi, Department of Internal Medicine, School of Life Dentistry at Niigata, The Nippon Dental University, Chuo-ku, Niigata 951-8580, Japan.
Masahiko YanoShogo Ohkoshi, Department of Internal Medicine, School of Life Dentistry at Niigata, The Nippon Dental University, Chuo-ku, Niigata 951-8580, Japan.
Yasunobu MatsudaShogo Ohkoshi, Department of Internal Medicine, School of Life Dentistry at Niigata, The Nippon Dental University, Chuo-ku, Niigata 951-8580, Japan.
Nippon Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A well-known tumor suppressor, p21, acts paradoxically by promoting tumor growth in some cellular conditions. These conflicting functions have been demonstrated in association with the HBx gene and in hepatocarcinogenesis. The molecular behavior of p21 depends on its subcellular localization. Nuclear p21 may inhibit cell proliferation and be proapoptotic, while cytoplasmic p21 may have oncogenic and anti-apoptotic functions. Because most typical tumor suppressive proteins also have different effects according to subcellular localization, elucidating the regulatory mechanisms underlying nucleo-cytoplasmic transport of these proteins would be significant and may lead to a new strategy for anti-hepatocellular carcinoma (HCC) therapy. Chromosome region maintenance 1 (CRM1) is a major nuclear export receptor involved in transport of tumor suppressors from nucleus to cytoplasm. Expression of CRM1 is enhanced in a variety of malignancies and in vitro studies have shown the efficacy of specific inhibition of CRM1 against cancer cell lines. Interestingly, interferon may keep p21 in the nucleus; this is one of the mechanisms of its anti-hepatocarcinogenic function. Here we review the oncogenic property of p21, which depends on its subcellular localization, and discuss the rationale underlying a new strategy for HCC treatment and prevention.

Indexed as

Active Transport, Cell NucleusAnimalsAntineoplastic AgentsBiomarkers, TumorCarcinoma, HepatocellularCell Transformation, NeoplasticCyclin-Dependent Kinase Inhibitor p21Drug DesignExportin 1 ProteinHumansKaryopherinsLiver NeoplasmsMolecular Targeted TherapyOncogene ProteinsReceptors, Cytoplasmic and NuclearSignal TransductionAntineoplastic AgentsBiomarkers, TumorCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21Exportin 1 ProteinKaryopherinsOncogene ProteinsReceptors, Cytoplasmic and NuclearTumor Suppressor ProteinsChromosome region maintenance 1HBxHepatocellular carcinomaInterferonNucleo-cytoplasmic exportOncogenep21Selective inhibitors of nuclear exportSubcellular localizationTumor suppressors

Identifiers

PMID26576099
PMCPMC4641132
OpenAlexW2176519545

What OpenQuestion holds

Textmetadata
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.