Evidence map›Paper›PMID 27050512›Full record

ArticleCell reports2016

Tumor-Induced Hyperlipidemia Contributes to Tumor Growth.

Jianfeng Huang, Lena Li, Jihong Lian, Silvia Schauer, Paul W Vesely, Dagmar Kratky, Gerald Hoefler, Richard Lehner

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.

  1. Pooled it
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  12. The evolving landscape of PCSK9 inhibition in cancer.European journal of pharmacology · 2023
    Review
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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

8 authors at 2 institutions in 2 countries.

Jianfeng HuangInstitute of Pathology, Medical University of Graz, 8010 Graz, Austria; Group on Molecular and Cell Biology of Lipids, University of Alberta, Edmonton, AB T6G 2R3, Canada.
Lena LiGroup on Molecular and Cell Biology of Lipids, University of Alberta, Edmonton, AB T6G 2R3, Canada; Department of Pediatrics, University of Alberta, Edmonton, AB T6G 2R3, Canada.
Jihong LianGroup on Molecular and Cell Biology of Lipids, University of Alberta, Edmonton, AB T6G 2R3, Canada; Department of Pediatrics, University of Alberta, Edmonton, AB T6G 2R3, Canada.
Silvia SchauerInstitute of Pathology, Medical University of Graz, 8010 Graz, Austria.
Paul W VeselyInstitute of Pathology, Medical University of Graz, 8010 Graz, Austria; Institute of Molecular Biosciences, Karl Franzens University of Graz, 8010 Graz, Austria.
Dagmar KratkyInstitute of Molecular Biology and Biochemistry, Center of Molecular Medicine, Medical University of Graz, 8010 Graz, Austria.
Gerald HoeflerInstitute of Pathology, Medical University of Graz, 8010 Graz, Austria. Electronic address: gerald.hoefler@medunigraz.at.
Richard LehnerGroup on Molecular and Cell Biology of Lipids, University of Alberta, Edmonton, AB T6G 2R3, Canada; Department of Pediatrics, University of Alberta, Edmonton, AB T6G 2R3, Canada. Electronic address: richard.lehner@ualberata.ca.
Medical University of Graz · ATUniversity of Alberta · CA

Funding

Austrian Science Fund FWF F 3013Austrian Science Fund FWF W 1226CIHR MOP-69043
6 · The paper itself

Abstract

The known link between obesity and cancer suggests an important interaction between the host lipid metabolism and tumorigenesis. Here, we used a syngeneic tumor graft model to demonstrate that tumor development influences the host lipid metabolism. BCR-Abl-transformed precursor B cell tumors induced hyperlipidemia by stimulating very low-density lipoprotein (VLDL) production and blunting VLDL and low-density lipoprotein (LDL) turnover. To assess whether tumor progression was dependent on tumor-induced hyperlipidemia, we utilized the VLDL production-deficient mouse model, carboxylesterase3/triacylglycerol hydrolase (Ces3/TGH) knockout mice. In Ces3/Tgh(-/-) tumor-bearing mice, plasma triglyceride and cholesterol levels were attenuated. Importantly tumor weight was reduced in Ces3/Tgh(-/-) mice. Mechanistically, reduced tumor growth in Ces3/Tgh(-/-) mice was attributed to reversal of tumor-induced PCSK9-mediated degradation of hepatic LDLR and decrease of LDL turnover. Our data demonstrate that tumor-induced hyperlipidemia encompasses a feed-forward loop that reprograms hepatic lipoprotein homeostasis in part by providing LDL cholesterol to support tumor growth.

Indexed as

AnimalsB-LymphocytesCarboxylic Ester HydrolasesCell Line, TransformedCell ProliferationCell SurvivalChylomicronsFusion Proteins, bcr-ablHyperlipidemiasInsulinLipoproteins, VLDLLiverMice, Inbred C57BLMice, KnockoutModels, BiologicalNeoplasmsCarboxylic Ester HydrolasesChylomicronsFusion Proteins, bcr-ablInsulinLipoproteins, VLDLPcsk9 protein, mouseProprotein Convertase 9

Identifiers

PMID27050512
PMCPMC4984953
OpenAlexW2325424191

What OpenQuestion holds

Texttitle and abstract
LicenceCC BY-NC-ND
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.