Evidence map›Paper›PMID 24505470›Full record

ArticlePloS one2014

A regulatory feedback loop between HIF-1α and PIM2 in HepG2 cells.

Zhenhai Yu, Xiaoping Zhao, Yingying Ge, Teng Zhang, Liangqian Huang, Xiang Zhou, Lei Xie, Jianjun Liu, Gang Huang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  11. Chinese Herbs Interfering with Cancer Reprogramming Metabolism.Evidence-based complementary and alternative medicine : eCAM · 2016
    Review
  12. Review
  13. 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

9 authors at 4 institutions in 1 country.

Zhenhai YuSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Xiaoping ZhaoDepartment of Nuclear Medicine, Ren ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Yingying GeState Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, China.
Teng ZhangDepartment of Nuclear Medicine, Ren ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Liangqian HuangInstitute of Health Sciences, Shanghai Jiao Tong University School of Medicine (SJTUSM) & Shanghai Institutes for Biological Sciences (SIBS), Chinese Academy of Sciences (CAS), Shanghai, China.
Xiang ZhouDepartment of Nuclear Medicine, Ren ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Lei XieDepartment of Nuclear Medicine, Ren ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Jianjun LiuDepartment of Nuclear Medicine, Ren ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Gang HuangDepartment of Nuclear Medicine, Ren ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China ; School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China ; Institute of Health Sciences, Shanghai Jiao Tong University School of Medicine (SJTUSM) & Shanghai Institutes for Biological Sciences (SIBS), Chinese Academy of Sciences (CAS), Shanghai, China.
Shanghai Jiao Tong University · CNRenji Hospital · CNChinese Academy of Sciences · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To survive under hypoxic conditions, cancer cells remodel glucose metabolism to support tumor progression. HIF transcription factor is essential for cellular response to hypoxia. The underlying mechanism how HIF is constitutively activated in cancer cells remains elusive. In the present study, we characterized a regulatory feedback loop between HIF-1α and PIM2 in HepG2 cells. Serine/threonine kinase proto-oncogene PIM2 level was induced upon hypoxia in a HIF-1α-mediated manner in cancer cells. HIF-1α induced PIM2 expression via binding to the hypoxia-responsive elements (HREs) of the PIM2 promoter. In turn, PIM2 interacted with HIF-1α, especially a transactivation domain of HIF-1α. PIM2 as a co-factor but not an upstream kinase of HIF-1α, enhanced HIF-1α effect in response to hypoxia. The positive feedback loop between PIM2 and HIF-1α was correlated with glucose metabolism as well as cell survival in HepG2 cells. Such a regulatory mode may be important for the adaptive responses of cancer cells in antagonizing hypoxia during cancer progression.

Indexed as

Cell HypoxiaGene Expression Regulation, NeoplasticGlucoseHep G2 CellsHumansHypoxia-Inducible Factor 1, alpha SubunitNeoplasmsPromoter Regions, GeneticProtein Serine-Threonine KinasesProto-Oncogene MasProto-Oncogene ProteinsGlucoseHypoxia-Inducible Factor 1, alpha SubunitMAS1 protein, humanPIM2 protein, humanProtein Serine-Threonine KinasesProto-Oncogene MasProto-Oncogene Proteins

Identifiers

PMID24505470
PMCPMC3914973
OpenAlexW2093118363

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.