Evidence map›Paper›PMID 26814431›Full record

ArticleOncotarget2016

Fatty acid activated PPARγ promotes tumorigenicity of prostate cancer cells by up regulating VEGF via PPAR responsive elements of the promoter.

Farzad S Forootan, Shiva S Forootan, Xiaojun Gou, Jin Yang, Bichong Liu, Danqing Chen, Majed Saad Al Fayi, Waseem Al-Jameel, Philip S Rudland, Syed A Hussain and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 2 pooled it
5.6field-weighted citation impact, top 4% 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

58 citing papers in PubMed, 2 syntheses or guidelines pooled it, 105 citations in OpenAlex.

  1. Pooled it
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  11. Dual function of activated PPARγ by ligands on tumor growth and immunotherapy.Medical oncology (Northwood, London, England) · 2024
    Review
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  13. Frontiers in pharmacology · 2024
    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

11 authors at 2 institutions in 2 countries.

Farzad S ForootanMolecular Pathology Laboratory, Department of Molecular and Clinical Cancer Medicine, Liverpool University, Liverpool L69 3GA, United Kingdom.
Shiva S ForootanMolecular Pathology Laboratory, Department of Molecular and Clinical Cancer Medicine, Liverpool University, Liverpool L69 3GA, United Kingdom.
Xiaojun GouAntibiotics Research and Re-evaluation Key Laboratory, Sichuan Antibiotics Industrial Institute, Chengdu University, Chengdu 610081, China.
Jin YangUrology Department of Affiliated Hospital, Chengdu University, Chengdu 610081, China.
Bichong LiuDepartment of Pharmacology, School of Pharmacology and Bioengineering, Chengdu University, Chengdu 610081, China.
Danqing ChenMolecular Pathology Laboratory, Department of Molecular and Clinical Cancer Medicine, Liverpool University, Liverpool L69 3GA, United Kingdom.
Majed Saad Al FayiMolecular Pathology Laboratory, Department of Molecular and Clinical Cancer Medicine, Liverpool University, Liverpool L69 3GA, United Kingdom.
Waseem Al-JameelMolecular Pathology Laboratory, Department of Molecular and Clinical Cancer Medicine, Liverpool University, Liverpool L69 3GA, United Kingdom.
Philip S RudlandDepartment of Biochemistry, Liverpool University, Liverpool L69 3GA, United Kingdom.
Syed A HussainMolecular Pathology Laboratory, Department of Molecular and Clinical Cancer Medicine, Liverpool University, Liverpool L69 3GA, United Kingdom.
Youqiang KeMolecular Pathology Laboratory, Department of Molecular and Clinical Cancer Medicine, Liverpool University, Liverpool L69 3GA, United Kingdom.
University of Liverpool · GBChengdu University · CN

Funding

Medical Research Council G0801447Medical Research Council MC_PC_14110
6 · The paper itself

Abstract

In previous work, it is suggested that the excessive amount of fatty acids transported by FABP5 may facilitate the malignant progression of prostate cancer cells through a FABP5-PPARγ-VEGF signal transduction axis to increase angiogenesis. To further functionally characterise the FABP5-PPARγ-VEGF signal transduction pathway, we have, in this work, investigated the molecular mechanisms involved in its tumorigenicity promoting role in prostate cancer. Suppression of PPARγ in highly malignant prostate cancer cells produced a significant reduction (up to 53%) in their proliferation rate, invasiveness (up to 89%) and anchorage-independent growth (up to 94%) in vitro. Knockdown of PPARγ gene in PC3-M cells by siRNA significantly reduced the average size of tumours formed in nude mice by 99% and tumour incidence by 90%, and significantly prolonged the latent period by 3.5 fold. Results in this study combined with some previous results suggested that FABP5 promoted VEGF expression and angiogenesis through PPARγ which was activated by fatty acids transported by FABP5. Further investigations showed that PPARγ up-regulated VEGF expression through acting with the PPAR-responsive elements in the promoter region of VEGF gene in prostate cancer cells. Although androgen can modulate VEGF expression through Sp1/Sp3 binding site on VEGF promoter in androgen-dependent prostate cancer cells, this route, disappeared as the cells gradually lost their androgen dependency; was replaced by the FABP5-PPARγ-VEGF signalling pathway. These results suggested that the FABP5-PPARγ-VEGF signal transduction axis, rather than androgen modulated route, may be a more important novel therapeutic target for angiogenesis-suppression treatment of castration resistant prostate cancer.

Indexed as

AnimalsBinding SitesCell Line, TumorCell ProliferationCell Transformation, NeoplasticFatty Acid-Binding ProteinsFatty AcidsGene Expression Regulation, NeoplasticHumansHuman Umbilical Vein Endothelial CellsMaleMiceMice, Inbred BALB CMice, NudeNeoplasm InvasivenessNeovascularization, PathologicFABP5 protein, humanFatty Acid-Binding ProteinsFatty AcidsPPAR gammaRNA, Small InterferingVascular Endothelial Growth Factor AVEGFA protein, humanFABP5PPARγPPREprostate cancerVEGF

Identifiers

PMID26814431
PMCPMC4891043
OpenAlexW2287556702

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.