Evidence map›Paper›PMID 28116790›Full record

ArticleProteomics2017

Proteomics analyses of prostate cancer cells reveal cellular pathways associated with androgen resistance.

Naseruddin Höti, Punit Shah, Yingwei Hu, Shuang Yang, Hui Zhang

Open access · greenAbstract read
In one paragraph

Article in Proteomics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 22 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

5 authors at 1 institution in 1 country.

Naseruddin HötiDepartment of Pathology, Johns Hopkins University, Baltimore, MD, USA.
Punit ShahDepartment of Pathology, Johns Hopkins University, Baltimore, MD, USA.
Yingwei HuDepartment of Pathology, Johns Hopkins University, Baltimore, MD, USA.
Shuang YangDepartment of Pathology, Johns Hopkins University, Baltimore, MD, USA.
Hui ZhangDepartment of Pathology, Johns Hopkins University, Baltimore, MD, USA.
Johns 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

While significant advances have been made in the diagnosis and treatment of prostate cancer, each year tens of thousands of men still die from prostate cancer in the United States. Thus, greater understanding of cellular pathways and molecular basis of prostate cancer progression in the development of androgen resistance is needed to treat these lethal phenotypes. To dissect the mechanism of androgen resistance, we utilize a proteomics approach to study the development of androgen resistance in LNCaP prostate cancer cells. Our results showed the predominant involvement of metabolic pathways that were elevated in androgen resistance phenotype. We further found the amplification of PI3K/AKT pathway and the overexpression of proteasome proteins while the mitochondrial oxidation phosphorylation was severely hampered in castration-resistant LNCaP-95 cells compared to LNCaP cells. Interestingly, we also found the induction of Dicer, a cytoplasmic endoribonuclease microRNA regulator in the androgen-ablated LNCaP-95 prostate cancer cells. We verified some of these data by orthogonal methods including Western blot analysis and in castrated animal xenograft studies. To our knowledge, this is the first report showing induced expression of proteasome proteins in androgen ablation prostate cancer cells. If validated in clinical studies, the findings will have significant implications in understanding the complexity of biochemical recurrence in prostate cancer.

Indexed as

Signal TransductionAndrogensCell Line, TumorCell ShapeChromatography, LiquidDown-RegulationDrug Resistance, NeoplasmHumansMaleOxidative PhosphorylationPhosphatidylinositol 3-KinasesProstatic NeoplasmsProteasome Endopeptidase ComplexProteomicsProto-Oncogene Proteins c-aktSubcellular FractionsAndrogensPhosphatidylinositol 3-KinasesProteasome Endopeptidase ComplexProto-Oncogene Proteins c-aktAndrogen resistanceLC-MS/MSOxidative phosphorylationPI3K/AKTProteasome

Identifiers

PMID28116790
PMCPMC5516940
OpenAlexW2581170664

What OpenQuestion holds

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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.