Evidence map›Paper›PMID 23383245›Full record

ArticlePloS one2013

βKlotho suppresses tumor growth in hepatocellular carcinoma by regulating Akt/GSK-3β/cyclin D1 signaling pathway.

Xiaoming Ye, Yu Guo, Qi Zhang, Wenjie Chen, Xuefeng Hua, Wei Liu, Yang Yang, Guihua Chen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
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  9. Biomarkers in Glycogen Storage Diseases: An Update.International journal of molecular sciences · 2021
    Review
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  11. Article
  12. Article
  13. Frontiers in oncology · 2019
    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

8 authors at 3 institutions in 1 country.

Xiaoming YeDepartment of General Surgery, Lingnan Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.
Yu Guo
Qi Zhang
Wenjie Chen
Xuefeng Hua
Wei Liu
Yang Yang
Guihua Chen
Sun Yat-sen University · CNKey Laboratory of Guangdong Province · CNSun Yat-sen Memorial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

βKlotho is a regulator in multiple metabolic processes, while its role in cancer remains unclear. We found the expression of βKlotho was down-regulated in human hepatocellular carcinoma tissues compared with that in paired adjacent non-tumourous liver tissues. Hepatoma cells also showed decreased expression of βKlotho compared with normal hepatocyte cells. Reintroduction of βKlotho into hepatoma cells inhibited their proliferation. The anti-proliferative effect of βKlotho might be linked with G1 to S phase arrest, which was mediated by Akt/GSK-3β/cyclin D1 signaling, since forced expression βKlotho reduced the phosphorylation level of Akt and GSK-3β and induced down-regulation of cyclin D1. Furthermore, βKlotho overexpression could inhibit tumorgenesis, while constitutively activated Akt could override the suppressive effects of βKlotho in vivo. These data suggest βKlotho suppresses tumor growth in hepatocellular carcinoma.

Indexed as

Signal TransductionAdultAgedAnimalsCarcinoma, HepatocellularCell Cycle CheckpointsCell Line, TumorCell ProliferationCyclin D1Disease Models, AnimalFemaleGene Expression Regulation, NeoplasticGlucuronidaseGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansCyclin D1GlucuronidaseGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, mouseKlotho ProteinsProto-Oncogene Proteins c-akt

Identifiers

PMID23383245
PMCPMC3559476
OpenAlexW2063367338

What OpenQuestion holds

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Registered trials

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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.