Evidence map›Paper›PMID 25834102›Full record

ArticleOncotarget2015

PIM1 regulates glycolysis and promotes tumor progression in hepatocellular carcinoma.

Carmen Oi-ning Leung, Carmen Chak-lui Wong, Dorothy Ngo-yin Fan, Alan Ka-lun Kai, Edmund Kwok-kwan Tung, Iris Ming-jing Xu, Irene Oi-lin Ng, Regina Cheuk-lam Lo

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

41 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Article
  3. PIM1 kinase and its diverse substrate in solid tumors.Cell communication and signaling : CCS · 2024
    Review
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  5. Article
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  17. Energy Metabolism in the Inner Retina in Health and Glaucoma.International journal of molecular sciences · 2021
    Review
  18. Article
  19. Article
  20. 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

8 authors at 1 institution in 1 country.

Carmen Oi-ning LeungDepartment of Pathology, The University of Hong Kong, Hong Kong, China.
Carmen Chak-lui WongDepartment of Pathology, The University of Hong Kong, Hong Kong, China.
Dorothy Ngo-yin FanDepartment of Pathology, The University of Hong Kong, Hong Kong, China.
Alan Ka-lun KaiDepartment of Pathology, The University of Hong Kong, Hong Kong, China.
Edmund Kwok-kwan TungDepartment of Pathology, The University of Hong Kong, Hong Kong, China.
Iris Ming-jing XuDepartment of Pathology, The University of Hong Kong, Hong Kong, China.
Irene Oi-lin NgDepartment of Pathology, The University of Hong Kong, Hong Kong, China.
Regina Cheuk-lam LoDepartment of Pathology, The University of Hong Kong, Hong Kong, China.
University of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is characteristically one of the most rapidly proliferating tumors which outgrows functional blood supply and results in regional oxygen deprivation. Overexpression of PIM1, a serine/threonine kinase, has been identified recently in human cancers. Knowledge on PIM1 in HCC is however, scarce. By immunohistochemical analysis on 56 human primary HCC samples, we observed overexpression of PIM1 in 39% of the cases. In two independent cohorts of paired primary and extra-hepatic metastatic HCC tissues, PIM1 expression was higher (p=0.002) in the extra-hepatic metastatic HCC tissues as compared with the corresponding primary HCCs. PIM1 was markedly up-regulated in multiple HCC cell lines in hypoxic condition (1% O2) versus normoxia (20% O2). Silencing of PIM1 suppressed HCC cell invasion in vitro as compared to non-target control, and decreased HCC cell proliferation in vitro and tumor growth and metastatic potential in vivo. Knockdown of PIM1 significantly reduced glucose uptake by HCC cells and was associated with decreased levels of p-AKT and key molecules in the glycolytic pathway. Taken together, PIM1 is up-regulated by hypoxia in HCC and promotes tumor growth and metastasis through facilitating cancer cell glycolysis. Targeting PIM1 may have potential role in the management of HCC.

Indexed as

GlycolysisActive Transport, Cell NucleusAgedAged, 80 and overAnimalsCarcinoma, HepatocellularCell HypoxiaCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansHypoxia-Inducible Factor 1, alpha SubunitHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitPIM1 protein, humanProteasome Endopeptidase ComplexProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-pim-1HCCmetastasisPIM1

Identifiers

PMID25834102
PMCPMC4484426
OpenAlexW1500418465

What OpenQuestion holds

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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.