Evidence map›Paper›PMID 29339807›Full record

ArticleProstate cancer and prostatic diseases2018

Overexpression of α (1,6) fucosyltransferase in the development of castration-resistant prostate cancer cells.

Naseruddin Höti, Shuang Yang, Yingwei Hu, Punit Shah, Michael C Haffner, Hui Zhang

Open access · hybridAbstract read
In one paragraph

Article in Prostate cancer and prostatic diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

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  19. Fucosylation in Urological Cancers.International journal of molecular sciences · 2021
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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

6 authors at 2 institutions in 1 country.

Naseruddin HötiDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Shuang YangDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Yingwei HuDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Punit ShahDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Michael C HaffnerDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Hui ZhangDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA. huizhang@jhu.edu.
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

Shared Resource CoresP01HL107153 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI KASS, DAVID ALAN · 2011 to 2017
$16.8M
Proteome Characterization Center: A Genoproteomics Pipeline for Cance ResearchU24CA160036 · NCI · JOHNS HOPKINS UNIVERSITY · PI CHAN, DANIEL WANYUI, ZHANG, HUI · 2011 to 2016
$10.7M
Glycoprotein biomarkers for the early detection of aggressive prostate cancerU01CA152813 · NCI · JOHNS HOPKINS UNIVERSITY · PI ZHANG, HUI · 2010 to 2021
$6.2M
The Comprehensive Proteome Characterization Center at Johns Hopkins: High Precision Discovery and Confirmation of Genoproteomic TargetsU24CA210985 · NCI · JOHNS HOPKINS UNIVERSITY · PI CHAN, DANIEL WANYUI, ZHANG, HUI · 2016 to 2020
$5.3M
NCI NIH HHS U01 CA152813NCI NIH HHS U24 CA160036NCI NIH HHS U24 CA210985NHLBI NIH HHS P01 HL107153
6 · The paper itself

Abstract

Glycosylation is recognized as one of the most common modifications on proteins. Recent studies have shown that aberrant expression of α (1,6) fucosyltransferase (FUT8), which catalyzes the transfer of fucose from GDP-fucose to core-GlcNAc of the N-linked glycoproteins, modulates cellular behavior that could lead to the development of aggressive prostate cancer. While the relationship between the abnormal expression of FUT8 and glycoprotein fucosylation in different prostate cancer cells has been demonstrated, there is no evidence that shows dysregulated fucosylation might be involved in prostate cancer progression from androgen-dependent to castration-resistant prostate cancer. In this study, using a proteomics approach, we analyzed androgen-dependent and androgen-resistant LAPC4 cells and identified FUT8 to be significantly overexpressed in the androgen-resistant LAPC4 cells. These findings were independently confirmed in LAPC4 cells that were treated with non-steroidal anti-androgen (bicalutamide) and in the in vivo castrated tumor xenograft models. Similarly, we also demonstrated that overexpression of FUT8 might be responsible for the decreased PSA expression in prostate cancer specimens. To our knowledge, this is the first study reporting the functional role of fucosylated enzyme in the development of castration-resistant prostate cancer.

Indexed as

AndrogensAnilidesAnimalsCell Line, TumorCell MovementFucoseFucosyltransferasesGene Expression Regulation, NeoplasticHumansMaleMiceNitrilesProstatic Neoplasms, Castration-ResistantTosyl CompoundsXenograft Model Antitumor AssaysAndrogensAnilidesbicalutamideFucoseFucosyltransferasesGlycoprotein 6-alpha-L-fucosyltransferaseNitrilesTosyl Compounds

Identifiers

PMID29339807
PMCPMC5895601
OpenAlexW2783564763

What OpenQuestion holds

Textmetadata
LicenceTDM
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.