Evidence map›Paper›PMID 24220243›Full record

ArticleCancer research2014

Blocking eIF5A modification in cervical cancer cells alters the expression of cancer-related genes and suppresses cell proliferation.

Elisabeth Mémin, Mainul Hoque, Mohit R Jain, Debra S Heller, Hong Li, Bernadette Cracchiolo, Hartmut M Hanauske-Abel, Tsafi Pe'ery, Michael B Mathews

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

57 citing papers in PubMed, 105 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

9 authors at 1 institution in 1 country.

Elisabeth MéminAuthors' Affiliations: Departments of Biochemistry and Molecular Biology, Pathology and Laboratory Medicine, Obstetrics, Gynecology and Women's Health, and Medicine, New Jersey Medical School, Rutgers University, Newark, New Jersey.
Mainul Hoque
Mohit R Jain
Debra S Heller
Hong Li
Bernadette Cracchiolo
Hartmut M Hanauske-Abel
Tsafi Pe'ery
Michael B Mathews
Rutgers, The State University of New Jersey · US

Funding

Rutgers Mass Spectrometry Core for Integrative Neuroscience ResearchP30NS046593 · NINDS · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI LOBEL, PETER · 2004 to 2018
$9.9M
NINDS NIH HHS P30 NS046593
6 · The paper itself

Abstract

Cancer etiology is influenced by alterations in protein synthesis that are not fully understood. In this study, we took a novel approach to investigate the role of the eukaryotic translation initiation factor eIF5A in human cervical cancers, where it is widely overexpressed. eIF5A contains the distinctive amino acid hypusine, which is formed by a posttranslational modification event requiring deoxyhypusine hydroxylase (DOHH), an enzyme that can be inhibited by the drugs ciclopirox and deferiprone. We found that proliferation of cervical cancer cells can be blocked by DOHH inhibition with either of these pharmacologic agents, as well as by RNA interference-mediated silencing of eIF5A, DOHH, or another enzyme in the hypusine pathway. Proteomic and RNA analyses in HeLa cervical cancer cells identified two groups of proteins in addition to eIF5A that were coordinately affected by ciclopirox and deferiprone. Group 1 proteins (Hsp27, NM23, and DJ-1) were downregulated at the translational level, whereas group 2 proteins (TrpRS and PRDX2) were upregulated at the mRNA level. Further investigations confirmed that eIF5A and DOHH are required for Hsp27 expression in cervical cancer cells and for regulation of its key target IκB and hence NF-κB. Our results argue that mature eIF5A controls a translational network of cancer-driving genes, termed the eIF5A regulon, at the levels of mRNA abundance and translation. In coordinating cell proliferation, the eIF5A regulon can be modulated by drugs such as ciclopirox or deferiprone, which might be repositioned to control cancer cell growth.

Indexed as

Cell ProliferationGene Expression Regulation, NeoplasticAntifungal AgentsCiclopiroxDeferiproneEukaryotic Translation Initiation Factor 5AFemaleGene Expression Regulation, EnzymologicGene SilencingHeLa CellsHumansIron Chelating AgentsMixed Function OxygenasesNF-kappa BPeptide Initiation FactorsProtein Processing, Post-TranslationalAntifungal AgentsCiclopiroxDeferipronedeoxyhypusine hydroxylaseEukaryotic Translation Initiation Factor 5AIron Chelating AgentsMixed Function OxygenasesNF-kappa BPeptide Initiation FactorsPyridonesRNA-Binding Proteins

Identifiers

PMID24220243
PMCPMC4745653
OpenAlexW2103699686

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.