Evidence map›Paper›PMID 26878389›Full record

ArticleOncogenesis2016

Diet-induced alteration of fatty acid synthase in prostate cancer progression.

M Huang, A Koizumi, S Narita, T Inoue, N Tsuchiya, H Nakanishi, K Numakura, H Tsuruta, M Saito, S Satoh and 3 more

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2016. 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 12% 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, 39 citations in OpenAlex.

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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

13 authors at 2 institutions in 1 country.

M HuangDepartment of Urology, Akita University Graduate School of Medicine, Akita, Japan.
A KoizumiDepartment of Urology, Akita University Graduate School of Medicine, Akita, Japan.
S NaritaDepartment of Urology, Akita University Graduate School of Medicine, Akita, Japan.
T InoueDepartment of Urology, Akita University Graduate School of Medicine, Akita, Japan.
N TsuchiyaDepartment of Urology, Akita University Graduate School of Medicine, Akita, Japan.
H NakanishiResearch Center for Biosignal,Akita University Graduate School of Medicine, Akita, Japan.
K NumakuraDepartment of Urology, Akita University Graduate School of Medicine, Akita, Japan.
H TsurutaDepartment of Urology, Akita University Graduate School of Medicine, Akita, Japan.
M SaitoDepartment of Urology, Akita University Graduate School of Medicine, Akita, Japan.
S SatohDepartment of Urology, Akita University Graduate School of Medicine, Akita, Japan.
H NanjoDepartment of Clinical Pathology, Akita University Graduate School of Medicine, Akita, Japan.
T SasakiAMED-CREST, Japan Agency for Medical Research and Development (AMED), Tokyo, Japan.
T HabuchiDepartment of Urology, Akita University Graduate School of Medicine, Akita, Japan.
Akita University · JPJapan Agency for Medical Research and Development · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fatty acid synthase (FASN) is a cytosolic metabolic enzyme that catalyzes de novo fatty acid synthesis. A high-fat diet (HFD) is attributed to prostate cancer (PCa) progression, but the role FASN on HFD-mediated PCa progression remains unclear. We investigated the role of FASN on PCa progression in LNCaP xenograft mice fed with HFD or low-fat diet (LFD), in PCa cells, and in clinical PCa. The HFD promoted tumour growth and FASN expression in the LNCaP xenograft mice. HFD resulted in AKT and extracellular signal-regulated kinase (ERK) activation and 5' adenosine monophosphate-activated protein kinase (AMPK) inactivation. Serum FASN levels were significantly lower in the HFD group (P=0.026) and correlated inversely with tumour volume (P=0.022). Extracellular FASN release was enhanced in the PCa cells with phosphatidylinositol 3-kinase (PI3K)/mitogen-activated protein kinase (MAPK) inhibition and AMPK signalling activation. FASN inhibition resulted in decrease of PCa cell proliferation through PI3K/MAPK downregulation and AMPK activation. Furthermore, AMPK activation was associated with FASN downregulation and PI3K/MAPK inactivation. Clinically, high FASN expression was significantly associated with high Gleason scores and advanced pathological T stage. Moreover, FASN expression was markedly decreased in the PCa response to androgen deprivation therapy and chemotherapy. HFD modulates FASN expression, which may be an important mechanism in HFD-associated PCa progression. Furthermore, a critical stimulatory loop exists between FASN and the PI3K/MAPK system, whereas AMPK signalling was associated with suppression. These may offer appropriate targets for chemoprevention and cancer therapy in HFD-induced PCa.

Identifiers

PMID26878389
PMCPMC5154344
OpenAlexW2270766610

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.