Evidence map›Paper›PMID 32085441›Full record

ArticleCancers2020

A Comprehensive Analysis of FUT8 Overexpressing Prostate Cancer Cells Reveals the Role of EGFR in Castration Resistance.

Naseruddin Höti, Tung-Shing Lih, Jianbo Pan, Yangying Zhou, Ganglong Yang, Ashely Deng, Lijun Chen, Mingmimg Dong, Ruey-Bing Yang, Cheng-Fen Tu and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

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  20. Mass Spectrometry-Based Glycoproteomics and Prostate Cancer.International journal of molecular sciences · 2021
    Review
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 2 countries.

Naseruddin HötiDepartment of Pathology, Johns Hopkins School of Medicine, Baltimore, MD 21287, USA.
Tung-Shing LihDepartment of Pathology, Johns Hopkins School of Medicine, Baltimore, MD 21287, USA.
Jianbo PanDepartment of Pathology, Johns Hopkins School of Medicine, Baltimore, MD 21287, USA.
Yangying ZhouDepartment of Pathology, Johns Hopkins School of Medicine, Baltimore, MD 21287, USA.
Ganglong YangDepartment of Pathology, Johns Hopkins School of Medicine, Baltimore, MD 21287, USA.
Ashely DengDepartment of Pathology, Johns Hopkins School of Medicine, Baltimore, MD 21287, USA.
Lijun ChenDepartment of Pathology, Johns Hopkins School of Medicine, Baltimore, MD 21287, USA.
Mingmimg DongDepartment of Pathology, Johns Hopkins School of Medicine, Baltimore, MD 21287, USA.
Ruey-Bing YangInstitute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan.ORCID 0000-0003-3017-3714
Cheng-Fen TuInstitute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan.
Michael C HaffnerDepartment of Pathology, Johns Hopkins School of Medicine, Baltimore, MD 21287, USA.
Qing Kay LiDepartment of Pathology, Johns Hopkins School of Medicine, Baltimore, MD 21287, USA.
Hui ZhangDepartment of Pathology, Johns Hopkins School of Medicine, Baltimore, MD 21287, USA.
Johns Hopkins University · USInstitute of Biomedical Sciences, Academia Sinica · TW

Funding

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 CA210985NIH HHS U01CA152813, U24CA160036
6 · The paper itself

Abstract

The emergence of castration-resistance is one of the major challenges in the management of patients with advanced prostate cancer. Although the spectrum of systemic therapies that are available for use alongside androgen deprivation for treatment of castration-resistant prostate cancer (CRPC) is expanding, none of these regimens are curative. Therefore, it is imperative to apply systems approaches to identify and understand the mechanisms that contribute to the development of CRPC. Using comprehensive proteomic approaches, we show that a glycosylation-related enzyme, alpha (1,6) fucosyltransferase (FUT8), which is upregulated in CRPC, might be responsible for resistance to androgen deprivation. Mechanistically, we demonstrated that overexpression of FUT8 resulted in upregulation of the cell surface epidermal growth factor receptor (EGFR) and corresponding downstream signaling, leading to increased cell survival in androgen-depleted conditions. We studied the coregulatory mechanisms of EGFR and FUT8 expression in CRPC xenograft models and found that castration induced FUT8 overexpression associated with increased expression of EGFR. Taken together, our findings suggest a crucial role played by FUT8 as a mediator in switching prostate cancer cells from nuclear receptor signaling (androgen receptor) to the cell surface receptor (EGFR) mechanisms in escaping castration-induced cell death. These findings have clinical implication in understanding the role of FUT8 as a master regulator of cell surface receptors in cancer-resistant phenotypes.

Indexed as

alpha (1,6) fucosyltransferaseglycoproteomicsprostate cancerproteomics

Identifiers

PMID32085441
PMCPMC7072180
OpenAlexW3007293071

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.