Evidence map›Paper›PMID 24260413›Full record

ArticlePloS one2013

The contributions of HIF-target genes to tumor growth in RCC.

Ting Zhang, Xiaohua Niu, Lili Liao, Eun-Ah Cho, Haifeng Yang

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 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
1.9field-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

45 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. The Role of the PAX Genes in Renal Cell Carcinoma.International journal of molecular sciences · 2024
    Review
  7. Vitexin enhances radiosensitivity of mouse subcutaneous xenograft glioma by affecting the miR-17-5p/miR-130b-3p/PTEN/HIF-1α pathway.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2024
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Sensitivity ofProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  16. Article
  17. The Most CommonCancers · 2021
    Article
  18. Article
  19. Article
  20. The Role of Metabolic Factors in Renal Cancers.International journal of molecular sciences · 2020
    Review
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

5 authors at 5 institutions in 2 countries.

Ting ZhangTianjin Institute of Urology, Second Hospital of Tianjin Medical University, Tianjin, China.
Xiaohua Niu
Lili Liao
Eun-Ah Cho
Haifeng Yang
Cerner (United States) · USCleveland Clinic · USCleveland Clinic Lerner College of Medicine · USSecond Hospital of Tianjin Medical University · CNThomas Jefferson University · US

Funding

Investigation of HIF-dependent and -independent tumor suppressor functions of VHLR01CA155015 · NCI · THOMAS JEFFERSON UNIVERSITY · PI YANG, HAIFENG · 2012 to 2016
$1.6M
NCI NIH HHS CA155015NCI NIH HHS R01 CA155015
6 · The paper itself

Abstract

Somatic mutations or loss of expression of tumor suppressor VHL happen in the vast majority of clear cell Renal Cell Carcinoma, and it's causal for kidney cancer development. Without VHL, constitutively active transcription factor HIF is strongly oncogenic and is essential for tumor growth. However, the contribution of individual HIF-responsive genes to tumor growth is not well understood. In this study we examined the contribution of important HIF-responsive genes such as VEGF, CCND1, ANGPTL4, EGLN3, ENO2, GLUT1 and IGFBP3 to tumor growth in a xenograft model using immune-compromised nude mice. We found that the suppression of VEGF or CCND1 impaired tumor growth, suggesting that they are tumor-promoting genes. We further discovered that the lack of ANGPTL4, EGLN3 or ENO2 expression did not change tumor growth. Surprisingly, depletion of GLUT1 or IGFBP3 significantly increased tumor growth, suggesting that they have tumor-inhibitory functions. Depletion of IGFBP3 did not lead to obvious activation of IGFIR. Unexpectedly, the depletion of IGFIR protein led to significant increase of IGFBP3 at both the protein and mRNA levels. Concomitantly, the tumor growth was greatly impaired, suggesting that IGFBP3 might suppress tumor growth in an IGFIR-independent manner. In summary, although the overall transcriptional activity of HIF is strongly tumor-promoting, the expression of each individual HIF-responsive gene could either enhance, reduce or do nothing to the kidney cancer tumor growth.

Indexed as

Gene Expression Regulation, NeoplasticAngiopoietin-Like Protein 4AngiopoietinsAnimalsCarcinoma, Renal CellCell Line, TumorCyclin D1Disease Models, AnimalGene Knockout TechniquesGlucose Transporter Type 1HumansHypoxia-Inducible Factor 1Hypoxia-Inducible Factor-Proline DioxygenasesInsulin-Like Growth Factor Binding Protein 3MicePhosphopyruvate HydrataseAngiopoietin-Like Protein 4AngiopoietinsANGPTL4 protein, humanCyclin D1EGLN3 protein, humanGlucose Transporter Type 1Hypoxia-Inducible Factor 1Hypoxia-Inducible Factor-Proline DioxygenasesInsulin-Like Growth Factor Binding Protein 3Phosphopyruvate HydrataseReceptor, IGF Type 1Vascular Endothelial Growth Factor AVon Hippel-Lindau Tumor Suppressor Protein

Identifiers

PMID24260413
PMCPMC3832366
OpenAlexW2073731809

What OpenQuestion holds

Textmetadata
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.