Evidence map›Paper›PMID 29026202›Full record

ArticleScientific reports2017

Loss of ABHD5 promotes the aggressiveness of prostate cancer cells.

Guohua Chen, Guoli Zhou, Siddhesh Aras, Zhenhui He, Stephanie Lucas, Izabela Podgorski, Wael Skar, James G Granneman, Jian Wang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.5field-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

28 citing papers in PubMed, 35 citations in OpenAlex.

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  18. Adipose triglyceride lipase activity regulates cancer cell proliferation via AMP-kinase and mTOR signaling.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020
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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

9 authors at 3 institutions in 2 countries.

Guohua ChenDepartment of Pathology, Wayne State University, Detroit, MI, 48201, USA.
Guoli ZhouBiomedical Research Informatics Core, Clinical and Translational Sciences Institute, Michigan State University, East Lansing, MI, 48824, USA.
Siddhesh ArasCenter for Molecular Medicine and Genetics, Wayne State University, Detroit, MI, 48201, USA.
Zhenhui HeDepartment of Laboratory Medicine, Foshan University Medical College, Foshan, Guangdong, 528000, China.
Stephanie LucasDepartment of Pathology, Wayne State University, Detroit, MI, 48201, USA.
Izabela PodgorskiDepartment of Pharmacology, Wayne State University, Detroit, MI, 48201, USA.
Wael SkarDepartment of Pathology, Wayne State University, Detroit, MI, 48201, USA.
James G GrannemanCenter for Molecular Medicine and Genetics, Wayne State University, Detroit, MI, 48201, USA.
Jian WangDepartment of Pathology, Wayne State University, Detroit, MI, 48201, USA. jianwang@med.wayne.edu.
Wayne State University · USFoshan University · CNMichigan State University · US

Funding

Tumor Biology and Microenvironment (Program 1)P30CA022453 · NCI · WAYNE STATE UNIVERSITY · PI PAUL M STEMMER · 1985 to 2026
$68.4M
Analysis of Lipolytic Trafficking in Adipocytes.R01DK076629 · NIDDK · WAYNE STATE UNIVERSITY · PI James G Granneman, Christopher V Kelly · 2009 to 2026
$7.1M
Functional Role of Bone Marrow Adipocytes in Metastatic Prostate CancerR01CA181189 · NCI · WAYNE STATE UNIVERSITY · PI PODGORSKI, IZABELA · 2014 to 2018
$1.6M
NCI NIH HHS P30 CA022453NCI NIH HHS R01 CA181189NIDDK NIH HHS R01 DK076629
6 · The paper itself

Abstract

The accumulation of neutral lipids in intracellular lipid droplets has been associated with the formation and progression of many cancers, including prostate cancer (PCa). Alpha-beta Hydrolase Domain Containing 5 (ABHD5) is a key regulator of intracellular neutral lipids that has been recently identified as a tumor suppressor in colorectal cancer, yet its potential role in PCa has not been investigated. Through mining publicly accessible PCa gene expression datasets, we found that ABHD5 gene expression is markedly decreased in metastatic castration-resistant PCa (mCRPC) samples. We further demonstrated that RNAi-mediated ABHD5 silencing promotes, whereas ectopic ABHD5 overexpression inhibits, the invasion and proliferation of PCa cells. Mechanistically, we found that ABHD5 knockdown induces epithelial to mesenchymal transition, increasing aerobic glycolysis by upregulating the glycolytic enzymes hexokinase 2 and phosphofrucokinase, while decreasing mitochondrial respiration by downregulating respiratory chain complexes I and III. Interestingly, knockdown of ATGL, the best-known molecular target of ABHD5, impeded the proliferation and invasion, suggesting an ATGL-independent role of ABHD5 in modulating PCa aggressiveness. Collectively, these results provide evidence that ABHD5 acts as a metabolic tumor suppressor in PCa that prevents EMT and the Warburg effect, and indicates that ABHD5 is a potential therapeutic target against mCRPC, the deadly aggressive PCa.

Indexed as

1-Acylglycerol-3-Phosphate O-AcyltransferaseAcyltransferasesAerobiosisCell Line, TumorCell MovementCell ProliferationCell RespirationDown-RegulationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGene Knockdown TechniquesGene SilencingGlycolysisHEK293 CellsHumansLipase1-Acylglycerol-3-Phosphate O-AcyltransferaseABHD5 protein, humanAcyltransferasesLipasePNPLA2 protein, humanTriglycerides

Identifiers

PMID29026202
PMCPMC5638841
OpenAlexW2761038766

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.