Evidence map›Paper›PMID 16607286›Full record

ArticleOncogene2006

A crucial function of PDGF in TGF-beta-mediated cancer progression of hepatocytes.

J Gotzmann, A N M Fischer, M Zojer, M Mikula, V Proell, H Huber, M Jechlinger, T Waerner, A Weith, H Beug and 1 more

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed, 1 pooled it
8.0field-weighted citation impact, top 2% 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

104 citing papers in PubMed, 1 synthesis or guideline pooled it, 238 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Phytochemical Profiling and Anticancer Potential ofAnti-cancer agents in medicinal chemistry · 2026
    Article
  4. Hepatocellular carcinoma: signaling pathways and therapeutic advances.Signal transduction and targeted therapy · 2025
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
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  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. The roles of E3 ligases in Hepatocellular carcinoma.American journal of cancer research · 2022
    Review
  20. Review

44 more citing papers are in PubMed but not listed here.

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

11 authors at 3 institutions in 2 countries.

J GotzmannDepartment of Medicine I, Division: Institute of Cancer Research, Medical University of Vienna, Vienna, Austria.
A N M Fischer
M Zojer
M Mikula
V Proell
H Huber
M Jechlinger
T Waerner
A Weith
H Beug
W Mikulits
Medical University of Vienna · ATResearch Institute of Molecular Pathology · ATBoehringer Ingelheim (Germany) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polarized hepatocytes expressing hyperactive Ha-Ras adopt an invasive and metastatic phenotype in cooperation with transforming growth factor (TGF)-beta. This dramatic increase in malignancy is displayed by an epithelial to mesenchymal transition (EMT), which mimics the TGF-beta-mediated progression of human hepatocellular carcinomas. In culture, hepatocellular EMT occurs highly synchronously, facilitating the analysis of molecular events underlying the various stages of this process. Here, we show that in response to TGF-beta, phosphorylated Smads rapidly translocated into the nucleus and activated transcription of target genes such as E-cadherin repressors of the Snail superfamily, causing loss of cell adhesion. Within the TGF-beta superfamily of cytokines, TGF-beta1, -beta2 and -beta3 were specific for the induction of hepatocellular EMT. Expression profiling of EMT kinetics revealed 78 up- and 235 downregulated genes, which preferentially modulate metabolic activities, extracellular matrix composition, transcriptional activities and cell survival. Independent of the genetic background, platelet-derived growth factor (PDGF)-A ligand and both PDGF receptor subunits were highly elevated, together with autocrine secretion of bioactive PDGF. Interference with PDGF signalling by employing hepatocytes expressing the dominant-negative PDGF-alpha receptor revealed decreased TGF-beta-induced migration in vitro and efficient suppression of tumour growth in vivo. In conclusion, these results provide evidence for a crucial role of PDGF in TGF-beta-mediated tumour progression of hepatocytes and suggest PDGF as a target for therapeutic intervention in liver cancer.

Indexed as

Animalsbeta CateninCarcinoma, HepatocellularCell NucleusCyclin-Dependent Kinase Inhibitor p16Disease ProgressionHepatocytesHumansLiver NeoplasmsMesodermMiceMice, Inbred BALB CMice, KnockoutMice, SCIDPhosphorylationPlatelet-Derived Growth Factorbeta CateninCdkn2a protein, mouseCyclin-Dependent Kinase Inhibitor p16Platelet-Derived Growth FactorReceptor, Platelet-Derived Growth Factor alphaReceptors, Platelet-Derived Growth FactorSmad ProteinsTransforming Growth Factor betaTumor Suppressor Protein p14ARF

Identifiers

PMID16607286
OpenAlexW1986991531

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.